Biomedical subjects

F Boomsma

Publications and source records attributed to F Boomsma.

At least 91 records · Page 5Linked to original sources

PubMed1996

Effects of alprazolam and lorazepam on catecholaminergic and cardiovascular activity during supine rest, mental load and orthostatic challenge.

Effects of oral alprazolam (0.5 and 1 mg) and lorazepam (2 mg) on sympathetic adrenomedullary activity and sedation were studied during supine rest, mental load (Color Word Test, CWT) and active standing (OCT), in 12 male volunteers in a randomized double-blind placebo-controlled cross-over design. Compared to placebo, alprazolam significantly increased subjective sedation, reduced plasma adrenaline and noradrenaline concentrations and mean blood pressure (MBP) during supine rest, and attenuated plasma adrenaline responses during the CWT and the OCT; these effects during the CWT and OCT appeared to be dose-dependent. In comparison with lorazepam (2 mg), alprazolam (1 mg) showed reduced MBP levels during supine rest, whereas lorazepam showed a higher heart rate level during supine rest, a reduced plasma noradrenaline response to the OCT and a performance deterioration to the CWT. There were no differences between alprazolam (1 mg) and lorazepam regarding subjective sedation. Although the benzodiazepines were similar regarding their increase of sedation, alprazolam and lorazepam induced differential effects on sympathetic adrenomedullary activity during rest and stress, whereby suppression of adrenomedullary activity may be specific for alprazolam.

Adult↗

PubMed1996

No change in automatic function tests during uncomplicated haemodialysis.

Uraemic autonomic dysfunction is reckoned to participate in dialysis hypotension, but a clear relationship has not been established. However, autonomic function is usually tested at rest, and possibly autonomic dysfunction arises or worsens during dialysis. We therefore performed easily repeatable tests of efferent sympathetic function, that is static exercise test and parasympathetic function, that is heart rate variability during Valsalva manoeuvre and deep breathing, at successive stages of a standard haemodialysis session; before dialysis, 20 min after dialysis without ultrafiltration, after 3 h of dialysis combined with ultrafiltration, and 20 min after dialysis. Studies were performed in 22 patients on chronic haemodialysis on a cuprophane dialyser. The mean ultrafiltration volume was 2.2 +/- 0.61. We found that blood pressure elevation upon static exercise, and heart rate variability during Valsalva or deep breathing test remained unaltered at the various stages of dialysis. On past performance the patients were divided into hypotension prone (n = 6) or resistant (n = 16). Hypotension prone patients showed a greater blood pressure drop during dialysis, but also showed an appropriately enhanced heart rate acceleration. The occurrence of autonomic dysfunction was not elevated in this group, nor did such dysfunction develop along dialysis. Predialysis parasympathetic function tests were abnormal in 10 patients. These patients also showed an augmented intradialytic blood pressure decrease, but no enhanced acceleration in heart rate. Their parasympathetic dysfunction did not worsen during dialysis. Based upon the predialysis exercise test, low responding patients (blood pressure increase 5 +/- 2 mmHg, n = 11) were distinguished. These subjects were not characterized by a greater blood pressure decrease or different heart rate acceleration. Generally, the responses upon exercise, whether low or high, remained unaltered during dialysis. we conclude that haemodialysis has no systematic effect on autonomic function. Hypotension-prone patients are not distinguished by a disturbed predialytic or intradialytic autonomic blood pressure control.

Adult↗

PubMed1996

Cyclosporin A impairs the nocturnal blood pressure fall in renal transplant recipients.

In renal transplant recipients, hypertension and a diminished nocturnal blood pressure fall are frequently found. To investigate whether this diminished nocturnal blood pressure fall is related to the use of cyclosporin A or to other factors, such as the use of glucocorticoids, we measured 24-hour ambulatory blood pressure in 18 renal transplant recipients both before and 16 weeks after conversion from cyclosporin A to azathioprine. Renal blood flow and glomerular filtration rate were estimated from 131I-hippurate and 125I-iothalamate clearances, respectively, and plasma concentrations of renin, atrial natriuretic peptide, norepinephrine, prostaglandin E2, and thromboxane B2 were determined. During cyclosporin A treatment, mean 24-hour blood pressure was 117 +/- 3 mm Hg, and the nocturnal fall in blood pressure was 4 +/- 9 mm Hg. A nondipping diurnal blood pressure pattern was present in 13 patients. After conversion to azathioprine, mean 24-hour blood pressure decreased to 109 +/- 3 mm Hg (P < .001), the nocturnal fall increased to 9 +/- 6 mm Hg, and the number of patients with a nondipping diurnal blood pressure pattern decreased to 9. The nocturnal fall in heart rate (17 +/- 10 beats per minute) during cyclosporin A did not change after conversion. Body weight and plasma concentrations of norepinephrine and renin did not change. Plasma concentrations of prostaglandin E2 and thromboxane B2 decreased after conversion, as did plasma atrial natriuretic peptide. Renal blood flow and glomerular filtration rate increased after conversion. In conclusion, cyclosporin A appears to be involved in the disturbance of the circadian blood pressure rhythm in renal transplant recipients. Although the precise mechanism is unclear. the elevated plasma atrial natriuretic peptide and slightly suppressed plasma renin concentrations suggest that intravascular volume expansion may contribute to the observed hemodynamic alterations.

Adult↗

PubMed1995

Ba2+ replaces Ca2+/calmodulin in the activation of protein phosphatases and in exocytosis of all major transmitters.

Exocytosis from nerve terminals is triggered by depolarization-evoked Ca2+ entry, which also activates calmodulin and stimulates protein phosphorylation. Ba2+ is believed to replace Ca2+ in triggering exocytosis without activation of calmodulin and can therefore be used to unravel aspects of presynaptic function. We have analysed the cellular actions of Ba2+ in relation to its effect on transmitter release from isolated nerve terminals. Barium evoked specific release of amino acid transmitters, catecholamines and neuropeptides (EC50 0.2-0.5 mM), similar to K-/Ca(2+)-evoked release both in extent and kinetics. Ba(2+)-and Ca(2+)-evoked release were not additive. In contrast to Ca2+, Ba2+ triggered release which was insensitive to trifluoperizine and hardly stimulated protein phosphorylation. These observations are in accordance with the ability of Ba2+ to replace Ca2+ in exocytosis without activating calmodulin. Nevertheless, calmodulin appears to be essential for regular (Ca(2+)-triggered) exocytosis, given its sensitivity to trifluoperizine. Both Ba(2+)-and Ca(2+)-evoked release were blocked by okadaic acid. Furthermore, anti-calcineurin antibodies decreased Ba(2+)-evoked release. In conclusion, Ba2+ replaces Ca2+/calmodulin in the release of the same transmitter pool. Calmodulin-dependent phosphorylation appears not to be essential for transmitter release. Instead, our data implicate both Ca(2+)-dependent and -independent dephosphorylation in the events prior to neurotransmitter exocytosis.

Animals↗

PubMed1995

Sensitivity and specificity of a new ELISA method for determination of chromogranin A in the diagnosis of pheochromocytoma and neuroblastoma.

We have evaluated a new commercially available ELISA kit for determination of plasma chromogranin A with respect to its usefulness in the diagnosis of neuroendocrine tumors, mainly pheochromocytoma. Serum and differently anticoagulated plasmas gave different chromogranin A concentrations. Control values (n = 21) were 18.9 +/- 5.8 units/l. Chromogranin A values > 30.4 units/l (mean + 2 S.D.) were considered elevated. In 22 patients suspected of (but found not to have) pheochromocytoma and in 24 patients with renovascular hypertension, 18% were found to have elevated chromogranin A concentrations. In renovascular hypertension chromogranin A correlated positively with serum creatinine; chromogranin A was strongly elevated especially in chronic renal failure. In 45 patients with pheochromocytoma, 13 (29%) had chromogranin A concentrations within the normal range, as had 3 out of 11 patients with neuroblastoma (27%). In 13 pheochromocytoma patients with elevated chromogranin A, measurements were repeated after surgical removal of the tumor; values then all fell within the normal range. We conclude that measurement of chromogranin A adds little to already existing methods for the diagnosis of pheochromocytoma.

Adult↗

PubMed1995

Progression of mild untreated heart failure during six months follow-up and clinical and neurohumoral effects of ibopamine and digoxin as monotherapy. DIMT Study Group. Dutch Ibopamine Multicenter Trial.

There is increasing evidence that clinical deterioration in manifest chronic heart failure is related to both hemodynamic and neurohumoral factors. Only few data are available, however, on the progression of disease in its early stages, when treatment has not yet been initiated. The aim of this study was therefore to examine the changes in clinical and neurohumoral variables that occur over 6 months in patients with clinically stable and untreated heart failure, and to evaluate the influence of drugs that may affect these variables. Accordingly, we studied 64 patients with heart failure who were in New York Heart Association functional class II (88%) and III (12%). They were randomized to double-blind treatment with the oral dopamine agonist ibopamine (100 mg 3 times daily; n = 22), digoxin (0.25 mg once daily; n = 22) or placebo (n = 20). Their age (mean +/- SD) was 60 +/- 8 years, and left ventricular ejection fraction (mean +/- SD) was 0.33 +/- 0.08. Of the 64 patients, 56 (88%) completed the 6-month study period (p = NS between groups). Exercise time decreased in patients treated with placebo after 6 months (median -62 seconds; p < 0.05 vs baseline), but it increased with ibopamine (+48 seconds), and digoxin (+17 seconds; both p < 0.05 vs placebo). Plasma norepinephrine increased in the placebo group after 6 months (median + 31 pg/ml, p < 0.05 vs baseline), but decreased in patients receiving active drug treatment (ibopamine: -24 pg/ml, digoxin: -98 pg/ml, both p < 0.05 vs placebo). Plasma renin and aldosterone levels were unchanged after 6 months in the placebo group, but digoxin therapy slightly reduced plasma renin concentration (-5 microU/ml; p < 0.05 vs placebo).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

Determination of semicarbazide-sensitive amine oxidase activity in human plasma by high-performance liquid chromatography with fluorimetric detection.

We report here a simple and sensitive method for the measurement of semicarbazide-sensitive amine oxidase (SSAO) activity in human plasma. Benzaldehyde, generated during a 1-h incubation of plasma with benzylamine, is derivatized with the specific aldehyde reagent dimedone after prior deproteinization. Quantitation of the derivatization product is done by automated injection onto an isocratic high-performance liquid chromatographic system with fluorimetric detection. The assay shows good linearity and reproducibility (intra-assay C.V. 7%). Detection limit is 25 mU/l (= pmol/ml/min). In 51 healthy controls (age 49 +/- 13 yr, 20 males) the measured SSAO activity was 352 +/- 102 mU/l (mean +/- S.D.). A large number of samples (70-80) can easily be processed in one day by one technician.

Adult↗

PubMed1995

Dose-dependent separation of dopaminergic and adrenergic effects of epinine in healthy volunteers.

Epinine (N-methyl-dopamine, the active metabolite of ibopamine), is a full agonist at dopamine (DA)-receptors and alpha- and beta-adrenoceptors. To study whether in vivo DA-receptors mediated effects can be separated from alpha- and beta-adrenoceptor effects we compared in 10 male volunteers the effects of i.v. epinine (0.5; 1; 2; 4 micrograms/kg/min for 15 min each) on DA-receptor (changes in serum prolactin)- and alpha- and beta-adrenoceptor (changes in systolic [Psyst] and diastolic blood pressure [Pdiast] and heart rate)-mediated effects with those of dopamine before and after propranolol (5 mg i.v. 45 min pre-infusion), bisoprolol (15 mg p.o. 2 h pre-infusion) and domperidone (10 mg p.o. 1 h pre-infusion). At the 0.5 and 1 microgram doses of dopamine and epinine did not effect Psyst, Pdiast and heart rate but significantly decreased prolactin levels. At the higher dose both dopamine and epinine significantly increased Psyst and heart rate, while only epinine significantly increased Pdiast. In addition, both dopamine and epinine significantly increased diuresis and natriuresis; in contrast, only dopamine, but not epinine dose-dependently increased plasma noradrenaline levels. Domperidone did not affect dopamine- and epinine-evoked blood pressure- and heart rate-changes, but antagonized their prolactin-effects (at least at the lower doses). Bisoprolol and propranolol significantly reduced dopamine-induced Psyst- and heart rate-increases to about the same extent. Propranolol enhanced epinine-induced Psyst- and Pdiast-increases while bisoprolol reduced epinine-evoked Psyst-increase but not Pdiast-increase. Epinine-induced heart rate-increase was abolished by bisoprolol and was converted into heart rate-decrease by propranolol. We concluded that in 0.5 and 1 microgram doses (plasma levels of 20-80 nmol/l)epinine acts only at DA-receptors. Thus, ibopamine in therapeutically recommended doses (3 x 100 mg/day with peak plasma epinine-levels of 50-80 nmol/l) very likely activates only DA-receptors. In higher doses, however, epinine-like dopamine-activates alpha- and beta-adrenoceptors whereby epinine has a stronger alpha-adrenoceptor agonistic activity than dopamine. Moreover, part of the dopamine-effects are indirect via release of endogenous noradrenaline whereas epinine-effects do not appear to include an indirect component.

Adult↗

PubMed1995

Contrasting effects of peripheral decarboxylase inhibitors on plasma activity of aromatic-L-amino acid decarboxylase and semicarbazide-sensitive amine oxidase in Parkinson's disease.

The peripheral decarboxylase inhibitors benserazide and carbidopa, often administered in combination with L-dopa in the treatment of Parkinson's disease, are also very good inhibitors of semicarbazide-sensitive amine oxidase (SSAO). In untreated patients and in patients treated with L-dopa alone, plasma SSAO activity is normal. In patients treated with L-dopa plus benserazide or carbidopa (Madopar or Sinemnet), however, plasma SSAO activity is strongly inhibited, contrary to the paradoxical 3-fold increase in plasma aromatic-L-amino acid decarboxylase activity we reported previously. Single-dose and longitudinal studies show that the SSAO inhibition proceeds rapidly and increases even further to nearly complete inhibition after continued treatment, while aromatic-L-amino acid decarboxylase activity only transiently decreases after a single dose and increases slowly with continued treatment above pretreatment levels. Dialysis experiments confirm that the binding of benserazide to SSAO is irreversible, especially after chronic treatment. The lack of knowledge about the exact function of SSAO precludes definite conclusions about the effect of this chronic SSAO inhibition on patients. Careful follow-up studies of patients treated with Madopar or Sinemet might provide further information about the possible physiological role of SSAO.

Aged↗

PubMed1995

Cardiac chronotropic responsiveness to beta-adrenoceptor stimulation is not reduced in the elderly.

OBJECTIVES: This study evaluated cardiac beta-adrenoceptor responsiveness in the elderly. BACKGROUND: The hypothesis of reduced cardiac beta-adrenoceptor responsiveness in the elderly is based on a smaller increase in heart rate after administration of isoproterenol, a nonselective beta 1- and beta 2-adrenoceptor agonist. By means of dobutamine-stress-echocardiography we were able to retest the hypothesis more accurately because dobutamine is a relatively selective beta 1-adrenoceptor agonist with weak beta 2- and alpha-adrenoceptor stimulant activity that prevents baroreflex-mediated changes in heart rate. METHODS: After administration of stepwise incremental infusions of dobutamine, we measured heart rate and blood pressure responses in 360 patients who had no beta-adrenergic blocking agent therapy and no side effects during the stress test. For each patient we calculated the dose of dobutamine required to increase heart rate by 50% of the maximal heart rate during the highest dose of dobutamine. RESULTS: No relation was found between age and sensitivity to dobutamine (n = 293). Power analysis revealed that this negative finding was not the result of inadequate sample size. In contrast to the prevailing hypothesis, an increased heart rate response to dobutamine was found even in a subgroup of "healthy" elderly subjects (i.e., those without concomitant disease or acute myocardial ischemia, n = 67) that was not related to changes in blood pressure during stress. However, in subjects with acute ischemia (n = 109), smokers (n = 151) or patients with a history of a previous myocardial infarction (n = 148), dobutamine sensitivity was reduced in the elderly despite a diminished change in systolic blood pressure with advanced age during dobutamine infusion. This phenomenon could be explained by a decrease in efferent cardiac baroreflex sensitivity, as has been observed during acute myocardial ischemia. There were no age-related differences in plasma concentrations of dobutamine. CONCLUSIONS: No evidence for reduced beta-adrenoceptor responsiveness to dobutamine was found in "healthy" elderly subjects.

Aged↗

PubMed1995

Heart rate variability in patients with mild to moderate heart failure: effects of neurohormonal modulation by digoxin and ibopamine. The Dutch Ibopamine Multicenter Trial (DIMT) Study Group.

OBJECTIVES: This study assessed the effects of digoxin and ibopamine on variables of heart rate variability in relation to neurohormonal activation. BACKGROUND: Analysis of heart rate variability can be used to study the autonomic dysfunction that characterizes chronic heart failure. In the Dutch Ibopamine Multicenter Trial, patients with heart failure were found to have increased neurohormonal activation with placebo therapy but not with digoxin and ibopamine therapy. METHODS: We studied 59 patients with mild to moderate heart failure (mean [+/- SEM] age 60 +/- 1 years, mean ejection fraction 0.30 +/- 0.01). Patients were randomized to double-blind treatment with digoxin (0.25 mg [n = 22]), ibopamine (100 mg three times a day [n = 19]) or placebo (n = 18); background therapy consisted of furosemide (up to 80 mg). RESULTS: After 3 months, plasma norepinephrine levels had increased with placebo, whereas they decreased with digoxin (+31 vs. -60 pg/ml, respectively, p < 0.01). With ibopamine, nonsignificant decrease was observed (-27 pg/ml, p = 0.10). All variables of heart rate variability showed a deterioration in the placebo group. With digoxin, the percent differences between successive RR intervals > 50 ms (pNN50) increased (+ 1.7 +/- 0.9%, p < 0.01), along with absolute and normalized high frequency power (+ 40 +/- 33 ms2, p < 0.05 and + 2.4 +/- 1.7%, p < 0.01, respectively). These changes were observed during daytime hours only and were most pronounced in patients with the most impaired baseline heart rate variability. With ibopamine, nonsignificant trends similar to the changes with digoxin were observed. CONCLUSIONS: In patients with early stages of heart failure, digoxin may prevent a progressive deterioration in heart rate variability, whereas ibopamine does not show statistically significant effects. The changes in heart rate variability with digoxin parallel an observed decrease in neurohormonal activation. Digoxin apparently enhances cardiac vagal tone in the setting of neuroendocrine activation.

Aldosterone↗

PubMed1995

Plasma semicarbazide-sensitive amine oxidase activity is elevated in diabetes mellitus and correlates with glycosylated haemoglobin.

1. Semicarbazide-sensitive amine oxidase is a common name for a group of heterogeneous amine oxidases which are present in various mammalian tissues, especially in vascular smooth muscle cells, cartilage and adipose tissue, but also in plasma. 2. Plasma semicarbazide-sensitive amine oxidase activity was elevated in a group of 104 patients with insulin-dependent diabetes mellitus compared with normal control subjects (555 +/- 172 versus 352 +/- 102 m-units/l, P < 0.0005). 3. Plasma semicarbazide-sensitive amine oxidase activity was higher in subgroups with either retinopathy or nephropathy or both [583 +/- 116 (n = 34), 581 +/- 229 (n = 10) and 646 +/- 249 m-units/l (n = 19), respectively] than in the subgroup without overt complications [486 +/- 129 m-units/l (n = 41), P < 0.005]. 4. Plasma semicarbazide-sensitive amine oxidase activity was positively correlated with plasma glycosylated haemoglobin (r = 0.40; P < 0.0001) and with log urinary albumin excretion (r = 0.26; P < 0.025). 5. The possibility that semicarbazide-sensitive amine oxidase, by its conversion of endogenous amines like methylamine and aminoacetone into cytotoxic aldehydes, plays a role in the development of microvascular complications in diabetes mellitus, needs further investigation.

Adult↗

PubMed1995

N-terminal-specific anti-B-50 (GAP-43) antibodies inhibit Ca(2+)-induced noradrenaline release, B-50 phosphorylation and dephosphorylation, and calmodulin binding.

B-50 (GAP-43) is a presynaptic protein kinase C (PKC) substrate implicated in the molecular mechanism of noradrenaline release. To evaluate the importance of the PKC phosphorylation site and calmodulin-binding domain of B-50 in the regulation of neurotransmitter release, we introduced two monoclonal antibodies to B-50 into streptolysin O-permeated synaptosomes isolated from rat cerebral cortex. NM2 antibodies directed to the N-terminal residues 39-43 of rat B-50 dose-dependently inhibited Ca(2+)-induced radiolabeled and endogenous noradrenaline release from permeated synaptosomes. NM6 C-terminal-directed (residues 132-213) anti-B-50 antibodies were without effect in the same dose range. NM2 inhibited PKC-mediated B-50 phosphorylation at Ser41 in synaptosomal plasma membranes and permeated synaptosomes, inhibited 32P-B-50 dephosphorylation by endogenous synaptosomal phosphatases, and inhibited the binding of calmodulin to synaptosomal B-50 in the absence of Ca2+. Similar concentrations of NM6 did not affect B-50 phosphorylation or dephosphorylation or B-50/calmodulin binding. We conclude that the N-terminal residues 39-43 of the rat B-50 protein play an important role in the process of Ca(2+)-induced noradrenaline release, presumably by serving as a local calmodulin store that is regulated in a Ca(2+)- and phosphorylation-dependent fashion.

Animals↗

PubMed1995

Hemodynamic and biochemical effects of the AT1 receptor antagonist irbesartan in hypertension.

We studied the hemodynamic, neurohumoral, and biochemical effects of the novel angiotensin type 1 (AT1) receptor antagonist irbesartan in 86 untreated patients with essential hypertension on a normal sodium diet. According to a double-blind parallel group trial, patients were randomized to a once-daily oral dose of the AT1 receptor antagonist (1, 25, or 100 mg) or placebo after a placebo run-in period of 3 weeks. Randomization medication was given for 1 week. Compared with placebo, 24-hour ambulatory blood pressure did not change with the 1-mg dose, and it fell (mean and 95% confidence interval) by 7.0 (4.2-9.8)/6.1 (3.9-8.1) mm Hg with the 25-mg dose and by 12.1 (8.1-16.2)/7.2 (4.9-9.4) mm Hg with the 100-mg dose. Heart rate did not change during either dose. With the 25-mg dose, the antihypertensive effect was attenuated during the second half of the recording, and with the 100-mg dose, it was maintained for 24 hours. Baseline values of renin and the antihypertensive response to the 25- and 100-mg doses were well correlated (r = .68, P < .01). Renin did not change with the 1-mg dose, but it rose threefold to fourfold with the 25-mg dose and fourfold to fivefold with the 100-mg dose 4 to 6 hours after administration. With the 100-mg dose, renin was still elevated twofold 24 hours after dosing. The changes in renin induced by the AT1 receptor antagonist were associated with parallel increments in angiotensin I and angiotensin II. Aldosterone, despite AT1 receptor blockade, did not fall.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Spectral analysis of hemodynamics during infusions of epinephrine and norepinephrine in men.

Spectral analysis of fluctuations in heart rate (HR) and arterial blood pressure (BP) during a 6-h infusion of epinephrine (15 ng.kg-1.min-1) or norepinephrine (30 ng.kg-1.min-1) in 10 normotensive males was used to analyze effects of peripheral sympathetic nervous system activity and adrenal medullary discharge on cardiovascular variability. Power spectra were calculated for each 5-min period for HR, systolic BP, and diastolic BP to yield power values for three frequency bands: low (0.02-0.06 Hz), mid (0.07-0.14 Hz), and high (0.15-0.40 Hz). Infusion of epinephrine and norepinephrine induced plasma concentrations of epinephrine and norepinephrine, respectively, within the high physiological range. Spectral analysis showed that low-frequency fluctuations of BP during infusions of epinephrine and midfrequency fluctuations of BP during infusion of norepinephrine changed in opposite directions. These fluctuations may represent different components of short-term cardiovascular control mechanisms during situations that mimic increased sympathoadrenal activity. No changes were observed in HR fluctuations or high-frequency fluctuations of BP after either catecholamine. Our data imply that changes in concentrations of circulating catecholamines cannot be unequivocally labeled as indexes of an altered sympathoadrenal involvement in short-term cardiovascular control.

Adult↗

PubMed1994

Arterial baroreflex control of renal hemodynamics in humans.

BACKGROUND: Control of renal hemodynamics by the arterial baroreflex has never been proved in humans. Apart from the physiological viewpoint, this issue is relevant because altered baroreflex function has been implicated in the pathogenesis of human hypertension. METHODS AND RESULTS: Renal function studies were performed in seated healthy volunteers (n = 12; age range, 20 to 34 years) during sustained neck suction at -60 mm Hg, aiming to selectively activate the carotid sinus arterial baroreceptors. Two protocols were followed. One group of 6 volunteers taking a 20 mmol/d sodium diet underwent 90 minutes of neck suction. Compared with a time-control study, neck suction decreased arterial pressure and heart rate; increased glomerular filtration rate (inulin clearance) from 104 +/- 6 to 114 +/- 8 mL/min (P < .01), renal plasma flow (para-aminohippurate clearance) from 616 +/- 52 to 665 +/- 42 mL/min (P < .01), and renal blood flow (from 1120 +/- 95 to 1209 +/- 77 mL/min, P < .01); and decreased renal vascular resistance (from 86 +/- 8 to 76 +/- 6 mm Hg.min.L-1, P < .01). Neck suction had no effect on plasma renin activity, aldosterone, atrial natriuretic peptide, catecholamines, and renal sodium excretion. The other 6 volunteers took a normal sodium diet and underwent sustained neck suction for 60 minutes. In this group, no effects on renal hemodynamics could be discerned, despite a modest decrease in blood pressure and heart rate. CONCLUSIONS: These data show, for the first time, that the arterial baroreflex is involved in the control of renal hemodynamics in humans. However, basal arterial baroreflex control of renal hemodynamics is probably low, and arterial baroreflex activation with subsequent renal vasorelaxation may be found only in conditions in which basal arterial baroreflex control of kidney function is significant, as is presumably the case in seated sodium-restricted subjects.

Adult↗

PubMed1994

Diurnal variation of blood pressure in patients with catecholamine-producing tumors.

To investigate the role of plasma catecholamines in diurnal blood pressure variation, invasive 24-h ambulatory blood pressure recordings (Oxford technique) were performed on 10 untreated patients; all had increased plasma concentrations of norepinephrine (mean 27.3; range 2.50 to 134.6 nmol/L) or epinephrine (mean 13.5; range 0.13 to 96.6 nmol/L) either attributable to a pheochromocytoma (n = 7) or a paraganglioma (n = 3). The nocturnal change in blood pressure was calculated as the percentage difference of blood pressure between night (midnight to 6 AM) and day (8 AM to 10 PM). The group average nocturnal change in blood pressure was 12.4%, ranging from a 32.0% decrease to a 2.8% increase, whereas the average nocturnal fall in heart rate was 18.6%, ranging from 2.2% to 33.4%. Although the nocturnal change in blood pressure was not significantly correlated with plasma values of norepinephrine (r = 0.60) or total catecholamines (r = 0.54), no nocturnal decrease in blood pressure occurred in the two patients with a plasma norepinephrine level of > 55 nmol/L. Recordings of three patients, all with a pheochromocytoma showed several paroxysms of blood pressure elevations, which lasted 18 to 47 min and had an amplitude of 32 to 94 mm Hg. In two cases these elevations had a true cyclic character. Our findings indicate that patients with a catecholamine-producing tumor may exhibit a normal diurnal blood pressure variation with a decrease in blood pressure during the night, suggesting that factors responsible for this diurnal variation remain operative in this condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Effects of DDAVP on renal hemodynamics and renin secretion in subjects with essential hypertension.

Intravenous (i.v.) infusion of the selective vasopressin (V2) agonist 1-desamino-8-D-arginine vasopressin (DDAVP, Desmopressin) in humans causes a fall in blood pressure, an increase in heart rate, and a rise in plasma renin and noradrenaline. The present study was designed to demonstrate the vasodilatory properties of DDAVP in the renal circulation and to describe the effect of DDAVP on renin secretion. Seven male subjects (31-63 years) with hypertension, who showed no signs of renal parenchymal disease, received an i.v. infusion of DDAVP (400 ng/kg in 10 minutes). They were studied at the time they were undergoing renal vein renin sampling and renal angiography as part of the diagnostic work-up of their hypertension. 131I-Hippurate clearance was used to measure effective renal plasma flow (ERPF). True renal plasma flow was calculated as ERPF divided by the renal extraction ratio of 131I-hippurate. 125I-Thalamate clearance was used to measure glomerular filtration rate (GFR). Measurements were made before and 15-20 minutes after administration of DDAVP. Angiography was performed in the same session after the last blood samples had been collected. In all patients the renal arteries were normal and the extraction ratios of 131I-hippurate and 125I-thalamate (Ehip, Ethal) were not different for the left and right kidney, and in all seven patients a diagnosis of essential hypertension was made. After DDAVP systolic blood pressure decreased by 14.4 mmHg (2.0-26.8) (mean, 95% confidence interval, p < 0.05). Diastolic blood pressure decreased by 12.1 mmHg (2.9-21.7, p < 0.01). Heart rate increased by 17.5 bpm (11.7-23.2, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗