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Biomedical subjects

H G Predel

Publications and source records attributed to H G Predel.

At least 37 records · Page 2Linked to original sources
PubMed1994

ACE inhibition and physical exercise: studies on physical work capacity, energy metabolism, and maximum oxygen uptake in well-trained, healthy subjects.

We investigated the effects of the angiotensin-converting enzyme (ACE) inhibitor trandolapril (2 mg/o.d.) on the physical work capacity (PWC), the received perception of exertion (RPE), as well as parameters determining physical performance (i.e., energy metabolism, lactate production, and oxygen uptake) in well-trained, healthy subjects. Twenty male sports students underwent a bicycle spiroergometry until exhaustion to determine maximum work load, maximum oxygen uptake, lactate threshold, and parameters of energy metabolism. The identical protocol was repeated after a 14-day treatment period with 2 mg of trandolapril o.d. or placebo. Treatment with the ACE inhibitor did not significantly alter maximum PWC, RPE, 4.0 mmol/L lactate threshold, heart rate, maximum oxygen uptake, plasma levels of total cholesterol, triglycerides, free fatty acids, glucose, insulin, cortisol, and human growth hormone. In the presence of the ACE inhibitor, the exercise-induced increase in systolic blood pressure was moderately (n.s.) blunted (204 +/- 7 versus 192 +/- 7 mm Hg). Treatment with the ACE inhibitor did not impair physical performance and RPE. This favorable profile of action was accompanied by no alterations in maximum oxygen uptake and parameters of energy metabolism at all levels of exercise intensity. Therefore, it may be concluded that antihypertensive treatment with an ACE inhibitor should be primarily considered in physically active patients.

Adult↗
PubMed1994

Lisinopril versus slow release nifedipine in patients with essential hypertension: a multicentre study.

The present study was performed to investigate the efficacy and safety of the angiotensin converting enzyme (ACE) inhibitor lisinopril compared with those of the calcium channel blocker nifedipine in 293 patients with mild to moderate essential hypertension (supine diastolic blood pressure (DBP) 95-115 mmHg) in a multicentre, randomised, double-blind parallel group study after a two week single-blind placebo run-in period. Thus, the haemodynamic effects as well as side-effects during antihypertensive treatment were examined in 146 patients receiving lisinopril (20 mg once daily) and in 147 patients receiving slow release nifedipine (20 mg twice daily) who entered the six weeks' treatment period. From the analysis of efficacy one patient from the lisinopril and two patients from the nifedipine groups were excluded because their supine DBP after run-in was < 95 mmHg. Adverse reactions, mostly transient during the initial treatment period, and withdrawals occurred in six (4.1%) and three (2.1%) patients of the lisinopril group and in 12 (8.2%; NS) and three (2.0%) patients of the nifedipine group, respectively. After the six weeks' treatment period the lisinopril group showed 19 nonresponders (supine DBP > or = 95 mmHg) of the remaining 142 patients and the nifedipine group revealed 20 nonresponders of the remaining 142 patients. Initial supine and standing heart rates were similar in both groups. Supine heart rate fell significantly in the lisinopril group, whereas standing heart rate in this group and supine and standing heart rates in the nifedipine group did not change significantly with treatment. Thus, lisinopril proved to be as effective and safe as nifedipine with responder rates of 86.6% and 85.9%, respectively.

Blood Cell Count↗
PubMed1992

Implications of pulsatile stretch on growth of saphenous vein and mammary artery smooth muscle.

Internal mammary artery (IMA) coronary bypass grafts have a higher patency than saphenous vein (SV) grafts. Intimal hyperplasia and occlusion of venous grafts result from smooth muscle proliferation. Mechanical factors, such as pulsatile stretch, are potential mediators of this process. Smooth muscle cells from IMA and SV were cultured on deformable membranes and exposed to pulsatile stretch (60 cycles/min). This stimulus increased 3H-thymidine incorporation into venous (a two-fold increase) but not arterial smooth muscle cells after 24 h. Smooth muscle cell numbers from SV, but not IMA, were increased (p less than 0.05) after 6 days of stretch. Thus, pulsatile stretch stimulates smooth muscle cell proliferation in SV, but not IMA, and may contribute to venous bypass graft disease.

Cell Division↗
PubMed1992

Intranasal application of atrial natriuretic peptide and 1-deamino-d-arginine vasopressin in healthy volunteers. Hemodynamic, hormonal, and renal excretory effects.

In the present study we investigated the effects of an intranasal administration of 25 micrograms alpha-human atrial natriuretic peptide (alpha-hANP) dissolved in 0.2 mL 0.9% saline on renal excretory function, blood pressure (BP), heart rate (HR), and also its interaction with the renal effects of 20 micrograms deamino-d-arginine vasopressin (d-DAVP) in 10 healthy volunteers. After two 30-min control periods plasma concentrations of ANP and cGMP rose significantly from 14.8 +/- 1.8 pmol/L and 5.9 +/- 0.3 pmol/mL to 23.3 +/- 2.3 pmol/L and 6.6 +/- 0.4 pmol/mL (P less than .05), respectively within 30 min after ANP administration. The levels returned to basal values after 60 min. Urinary cGMP excretion initially rose from 17.9 +/- 3.6 to 46.8 +/- 3.7 pmol/30 min and then returned to control values, whereas plasma renin activity and plasma aldosterone concentration decreased significantly after 30 and 60 min (P less than .05). Systolic and diastolic BP declined slightly by 8% and 7%, respectively, while HR remained unaltered. Urine flow rate and sodium excretion increased by 321% and 190%, respectively (P less than .05). These changes were also significant when data were compared with a time-matched placebo study performed on the preceding day with intranasal administration of 0.2 mL 0.9% saline alone. After 48 h the protocol was repeated but 20 micrograms d-DAVP was administered intranasally 120 min before an intranasal application of 25 micrograms alpha-hANP. Within 120 min d-DAVP had reduced urine flow by approximately 50% (P less than .05), while sodium excretion remained unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗
PubMed1991

Effects of atrial natriuretic peptide on systemic and renal hemodynamics and renal excretory function in patients with chronic renal failure.

We examined the effects of 60 min alpha-hANP infusion (24 ng/min/kg) on glomerular filtration rate (GFR), renal blood flow (RBF), cardiac index (CI) and blood pressure (BP) in 8 patients with chronic renal failure (CRF) with GFR ranging from 18 to 80 ml/min/1.73 m2 and in 8 control (C) subjects with normal renal function. Basal plasma levels of ANP and cGMP were elevated in CRF (ANP: 60.6 +/- 9.1 vs 13.6 +/- 1.9 pmol/l, p less than 0.05; cGMP: 14.3 +/- 2.9 vs 6.6 +/- 1.1 pmol/ml, p less than 0.05). During ANP infusion, peak levels of cGMP were higher in CRF than in C (27.5 +/- 3.2 vs. 17.3 +/- 1.3 pmol/ml, p less than 0.05). During ANP infusion, GFR increased in CRF by 70.7 +/- 4.2% from 34.5 +/- 6.8 to 57.4 +/- 9.9 ml/min/1.73 m2 (p less than 0.001) as compared to 16.2 +/- 1.4% in C (p less than 0.001 vs CRF). RBF increased in CRF by 43.6 +/- 6.4% and in C by 3.1 +/- 1.2% (p less than 0.01). Basal urinary sodium excretion (UNaV) was slightly lower in CRF than in C but rose to the same level in both groups during ANP infusion. In CRF, as opposed to C, UNaV remained elevated above baseline after the end of the infusion. The effect of ANP on fractional sodium excretion (FENa), however, was more pronounced in C.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Endogenous natriuretic and ouabain-like factors. Their roles in body fluid volume and blood pressure regulation.

An endogenous ouabain-like sodium pump inhibitor was demonstrated originally in serum or plasma of acutely extracellular fluid volume (ECFV) expanded animals and humans. Since then numerous studies have confirmed the presence of ouabain-like factor(s) (OLF) in blood, urine, cerebrospinal fluid, and various tissues including the heart and hypothalamus. Some of these OLFs represent well-known endogenous compounds, eg, free unsaturated fatty acids, which in vitro exhibit inhibition of transepithelial sodium transport, direct inhibition of the Na-K-ATPase enzyme, displacement of 3H-ouabain from its membrane receptor, and crossreaction with a digoxin antibody. Small molecular weight (MW) OLFs of yet unknown peptidic or nonpeptidic nature, which may be of hypothalamic origin, were also detected in various animal models of hypertension and in hypertensive patients. They may play a pathophysiological role especially in salt- and volume-dependent forms of hypertension. Our results show that OLFs increase basal and vasopressin-stimulated intracellular Ca2+ release in rat vascular smooth muscle cells in culture and in human platelets similar to the newly discovered endothelin. In addition, a natriuretic factor (natriuretic hormone) was detected by bioassay in plasma and urine, whose activity changes in parallel with sodium intake. We found that this natriuretic factor is associated with small peptides with a MW of less than 1,000. It is, however, unlikely that the two biological properties, ie, the ouabain-like and natriuretic activities, reside in a single compound. A number of circulating OLFs is certainly not identical with a humoral natriuretic factor. Nevertheless, there is increasing evidence for multiple interactions between OLF and the atrial natriuretic peptide (ANP).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Atrial natriuretic peptide in patients with essential hypertension. Hemodynamic, renal, and hormonal responses.

In six patients with essential hypertension (EH) and in six healthy volunteers (C) the effects of a 60-min intravenous (iv) infusion of human atrial natriuretic peptide (alpha-hANP) (24 ng/min/kg) on systemic and renal hemodynamics and renal excretory function were evaluated. Basal plasma ANP concentrations in patients with EH were higher (P less than .05) than in C (30.9 +/- 4.5 v14.0 +/- 1.7 pmol/L). Maximal effects of alpha-hANP infusion occurred after 30 to 60 min. Blood pressure (BP) declined from 154 +/- 5/109 +/- 4 to 139 +/- 7/94 +/- 4 in EH and from 117 +/- 1/72 +/- 2 to 106 +/- 1/65 +/- 3 mm Hg in C (P less than .05). Cardiac output (CO) increased transiently from 6.1 +/- 0.3 to 6.5 +/- 0.4 L/min in EH and from 6.8 +/- 0.3 to 7.2 +/- 0.5 L/min in C, whereas heart rate (HR) remained constant both in patients with EH and in C (69 +/- 3 to 72 +/- 5 and 60 +/- 3 to 63 +/- 3/min). The increases in urine flow and in urinary sodium excretion from 3.6 +/- 0.2 to 16.0 +/- 2.0 mL/min and from 230 +/- 33 to 1004 +/- 137 mumol/min, respectively, in EH were more pronounced than in C (from 3.9 +/- 1.0 to 8.4 +/- 0.8 mL/min and from 211 +/- 37 to 451 +/- 84 mumol/min); (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Plasma concentrations of endothelin in patients with abnormal vascular reactivity. Effects of ergometric exercise and acute saline loading.

We measured circulating concentrations of endothelin, a recently discovered vasoconstrictor peptide produced by vascular endothelial cells, in healthy subjects and in patients with abnormal vascular reactivity. Endothelin concentrations were determined by radio-immunoassay after extraction of plasma using Sep-Pak C-18 cartridges in healthy subjects (n = 20), in patients with diabetes mellitus type I (n = 10), in patients with mild to moderate essential hypertension (n = 12) and in non-dialyzed patients with stable chronic renal failure (n = 12). Plasma concentrations were similar in healthy controls, in diabetics and in hypertensive patients averaging 5.0 +/- 0.6 pg/ml, 4.7 +/- 0.2 pg/ml and 6.5 +/- 1.0 pg/ml, respectively. In contrast, plasma concentrations of endothelin were markedly elevated in patients with chronic renal failure averaging 16.6 +/- 2.9 pg/ml (p less than 0.005). No correlations were observed between serum creatinine concentrations ranging from 124 to 850 mumol/l or blood pressure and plasma concentrations of endothelin. Bicycle ergometric exercise in six healthy subjects and an acute modest i.v. saline load of 1,000 ml of 0.45% NaCl administered within 60 min in six patients with mild essential hypertension did not affect plasma concentrations of endothelin. Thus, it is unlikely that vascular synthesis of endothelin is related to acute physiological changes in systemic hemodynamics or to the circulatory and renal responses to acute extracellular fluid volume (ECFV) expansion. A potential role of endothelin, however, in the control of regional blood flow cannot be excluded. Elevated plasma concentrations of endothelin observed in patients with chronic renal failure require further investigations.

Adult↗
PubMed1990

Atrial natriuretic peptide in patients with diabetes mellitus type I. Effects on systemic and renal hemodynamics and renal excretory function.

In the present study the effects of 1 h intravenous infusion of alpha-human atrial natriuretic peptide (24 ng/min/kg) on systemic and renal hemodynamics and on renal excretory function were studied in six insulin-treated and metabolically well-controlled patients with diabetes mellitus (DM) type I and in six healthy control subjects (C). Basal plasma atrial natriuretic peptide (ANP) concentration was 14.6 +/- 2.0 in DM patients and 14.9 +/- 1.3 pmol/L in C and rose similarly in both groups to 87.1 +/- 22.1 and to 86.9 +/- 11.1 pmol/L, respectively, during alpha-hANP infusion (P less than .05). Maximal effects of alpha-hANP occurred between 30 and 60 min after the start of the infusion. Mean arterial pressure (MAP) (83 +/- 5 v 81 +/- 3 mm Hg), heart rate (HR) (63 +/- 2 v 64 +/- 4/min) and total peripheral resistance (TPR) (11 +/- 1 v 10 +/- 1 mm Hg.min/L) remained unaltered in patients with DM. In contrast, in C MAP and TPR decreased from 83 +/- 3 to 77 +/- 2 mm Hg and from 12 +/- 1 to 10 +/- 1 1 mm Hg.min/L, respectively (P less than .05), whereas HR increased from 53 +/- 2 to 59 +/- 3 beats/min (P less than .05). Cardiac output (CO) rose initially by 11% and by 9% in DM and C, respectively. Urine flow increased from 4.1 +/- 0.9 to 11.3 +/- 1.5 mL/min in DM patients and from 3.9 +/- 1.0 to 8.4 +/- 0.8 mL/min in C (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Kinin- and non-kinin-mediated interactions of converting enzyme inhibitors with vasoactive hormones.

The antihypertensive effect of inhibitors of the angiotensin I-converting enzyme (ACE = kininase II) results from their vasodilatory and natriuretic effects as well as their effect on baroreceptor function. In addition to the inhibition of systemic and local angiotensin II formation, other local hormonal systems may also be involved in this effect at multiple target sites. Thus, potentiation of the vasodilator and natriuretic kinin system following inhibition of kininase II is thought to contribute to the persistent hypotensive effect of ACE inhibitors despite normalization of circulating ACE activity. Although increased plasma bradykinin levels cannot be detected, we found that the enhanced kinin-dependent local vascular prostacyclin production can be blunted in vitro by aprotinin, a kallikrein inhibitor. ACE inhibition may affect the atrial natriuretic peptide (ANP) system as the renin-angiotensin system and ANP appear to play antagonistic roles at the peripheral and central nervous system levels. Inhibition of kallikrein or of kininase II were both shown to modulate the natriuretic and vasorelaxant effects of ANP. In hypertensive subjects, we found that ACE inhibition with blood pressure normalization reduces basal and stimulated plasma ANP and blunts the renal sodium excretion in response to saline loading. In contrast, we did not observe effects of acute ACE inhibition in healthy sodium-depleted volunteers on plasma vasopressin under basal conditions or in response to passive tilt. Finally, we investigated the interaction of ACE inhibition with substance P, a powerful endogenous diuretic and natriuretic peptide that may have a transmitter function in the baroreceptor reflex arch.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Angiotensin-converting enzyme inhibition in patients with essential hypertension.

The antihypertensive action of angiotensin-converting enzyme (ACE) inhibitors may be related to inhibition of systemic and local vascular angiotensin-II formation, to a potentiation of the local vascular kinin system with secondary stimulation of prostacyclin synthesis, and also to their effects on the central nervous system as well as on renal hemodynamics and excretory function. More detailed studies in patients with severe hypertension, previously not adequately controlled by conventional therapy with a diuretic, a beta-blocking agent and a vasodilator dihydralazine, showed that addition of the ACE inhibitor ramipril normalized systolic and diastolic blood pressure (BP) without hypotensive episodes or reflex tachycardia. ACE inhibition caused a change in the baroreceptor set point as we had previously demonstrated in healthy subjects, but baroreceptor sensitivity was not affected and the pressure response to exogenous norepinephrine remained unchanged by ACE inhibition. Despite the significant reduction in BP in our patients, endogenous creatinine clearance remained unaltered. Furthermore, the decrease in BP is accompanied by an initial natriuresis probably contributing to the BP-lowering effect of ACE inhibitors. Decreased proximal tubular reabsorption may include enhanced urate clearance reflected by a decrease in serum urate concentration which we observed despite continuous diuretic treatment. ACE inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. In our patients this resulted in a 10% decrease in urinary potassium excretion and a small rise in serum potassium concentration. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydroosmotic effect of vasopressin, thus resulting in a rise in free-water clearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1989

Effects of endothelin on sodium transport mechanisms: potential role in cellular Ca2+ mobilization.

The effects of endothelin on cellular Ca2+ mobilization were examined in cultured rat vascular smooth muscle cells (VSMC). Endothelin (10(-8)M) induced a rapid transient increase of [Ca2+]i from 77 +/- 3 to 104 +/- 5 nM (p less than .05) in VSMC. Preincubation (60 min) with endothelin (2 x 10(-6)M) increased basal [Ca2+]i from 77 +/- 3 to 105 +/- 8 nM (p less than .05). Preincubation with endothelin also enhanced vasopressin (10(-7)M)-stimulated peak levels of [Ca2+]i (528 +/- 20 nM vs 969 +/- 21 nM, p less than .01). Endothelin (10(-7)M) induced an intracellular alkalinization (7.18 +/- 0.03 vs 7.37 +/- 0.04, p less than .01) which was blocked by pretreatment with amiloride. The biphasic effects of endothelin on [Ca2+]i were similar to those of an endogenous inhibitor of Na-K-ATPase that we examined in a previous study. Therefore, we examined the effects of endothelin on Na-K-ATPase in an enzyme preparation from hog cerebral cortex. At high concentrations, endothelin (10(-5)M) inhibited Na-K-ATPase in vitro. Thus, endothelin may exert its vasoconstrictor effects at least in part via alterations of cellular Ca2+ mobilization in VSMC. While the rapid transient increase of [Ca2+]i appears to reflect intracellular Ca2+ mobilization, the sustained effect on [Ca2+]i may be related to an increase of intracellular sodium mediated by inhibition of Na-K-ATPase and/or more likely by stimulation of the Na+/H+-antiport.

Animals↗
PubMed1989

[Recurrent thrombophlebitis, weakness].

The 46-year-old woman was admitted with an acute inflammatory swelling of the left forearm. During the previous six months the patient had suffered from recurrent thromboses of the superficial veins associated with generalized physical weakness. The gynaecological history was remarkable for hypermenorrhea and metrorrhagia. On examination, the signs of an acute thrombophlebitis with concomitant lymphangitis were observed. In the lower right abdomen there was a palpable tumor. Laboratory findings showed a mild anemia and indices of inflammation. Subsequent procedures (abdominal sonography, gynaecological examination) further substantiated the suspicion of an underlying malignant process. Hysterectomy and histological examination revealed two different carcinomas of the right ovary and of the uterine cave. Already during the uncomplicated postoperative period the thrombophlebitis completely regressed.

Adenocarcinoma↗
PubMed1989

[Urticaria, pruritus].

A 53-year old patient was admitted because of severe urticaria and itching aggravating since 9 months. Laboratory findings like increased sedimentation rate and leucocytosis were suspicious for an infection-associated allergy or a paraneoplastic syndrome. After exclusion of a gastro-intestinal tumor search for the source of a possible infection was intensified by several fecal analyses and trophozoites were found indicating an infestation of the small bowel by Giardia lamblia. Finally lamblia were detected in duodenal aspirate. After therapy with metronidazole 3 x 400 mg/die for 10 days all parameters of infection were normalized and the patient was permanently relieved from symptoms.

Giardiasis↗
PubMed1989

Human atrial natriuretic peptide in non-dialyzed patients with chronic renal failure.

The role of human atrial natriuretic peptide (alpha-hANP) in the regulation of blood pressure (BP) and extracellular fluid volume (ECFV) remains elusive. This is of particular interest in chronic renal failure, in which first, increased sodium and water retention plays a major pathogenetic role in the development of hypertension, and second, altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. In the present study the relationship between renal function, BP, and circulating alpha-hANP was investigated in 16 non-dialyzed patients with stable chronic renal failure (CRF) without edema. Analysis of potential molecular heterogeneity of immunoreactive (ir) ANP was performed by gel permeation chromatography of plasma extracts from normotensive patients with CRF. Serum creatinine concentrations averaged 435 +/- 76 mumol/l ranging from 127 to 1187 mumol/l, systolic and diastolic BP averaged 158 +/- 4 and 94 +/- 2 mmHg, respectively. Plasma alpha-hANP concentrations ranged from 5 to 75 with a mean of 23 +/- 4 pmol/l as compared to a mean of 10 +/- 1 pmol/l in healthy volunteers (p less than 0.05). A significant linear correlation between plasma alpha-hANP and serum creatinine concentrations (r = 0.92) was observed; a weaker correlation was found between mean arterial pressure and alpha-hANP (r = 0.66). Chromatographic analysis revealed considerable amounts of higher molecular weight circulating ir-ANP, approximately 15,000 Da, in addition to the biologically active small mol wt ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Elevated plasma levels and heterogeneity of human atrial natriuretic peptide in patients with progressive chronic renal failure].

The role of human atrial natriuretic peptide (alpha-hANP) in chronic blood pressure (BP) and extracellular fluid volume (ECFV) regulation remains elusive. Hence, the role of alpha-hANP in chronic renal failure is of particular interest since in this pathological condition: (1) increased sodium and water retention plays a major pathogenetic role in the development of hypertension and (2) altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. To evaluate the relationship between the degree of renal insufficiency, BP and circulating alpha-hANP, we determined plasma alpha-hANP concentrations by radioimmunoassay in 16 nondialyzed patients with progressive chronic renal failure (CRF) of various degrees; subsequently analysis of potential molecular heterogeneity of immunoreactive (ir) ANP was performed by means of gel permeation of plasma extracts from patients with CRF without concomitant hypertension. Serum creatinine concentrations ranged from 127 to 1187 (435 +/- 76) mumol/l, systolic BP from 135 to 200 (158 +/- 4) and diastolic BP from 80 to 110 (94 +/- 2) mmHg, respectively. Plasma alpha-hANP concentrations ranged from 5 to 75 (23 +/- 4) pmol/l which was thus significantly higher as compared to 9 +/- 2 pmol/l found in healthy volunteers (p less than 0.05). A highly significant linear correlation between plasma alpha-hANP and serum creatinine concentrations (r = 0.92; p less than 0.01) was observed; a weaker correlation was found between mean arterial pressure and alpha-hANP (r = 0.66) and serum creatinine concentration (r = 0.59), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Baroreflex setting and sensitivity in normal subjects: effects of pharmacologic inhibition of the angiotensin I converting enzyme.

Arterial blood pressure, heart rate and the response of these hemodynamic parameters to exogenous norepinephrine were investigated in healthy volunteers (daily sodium intake of 150 mmol) during a control period and after a single oral dose of 5 mg of the angiotensin I converting enzyme (ACE) inhibitor ramipril (HOE 498). Norepinephrine was infused at doses of 0.1, 0.2 and 0.3 micrograms kg-1 min-1, each for 10 minutes, during control and 3 hours after ramipril administration. Exogenous norepinephrine induced a dose-dependent increase in mean arterial blood pressure from 76.4 +/- 0.9 mm Hg during control to 85.6 +/- 1.5, 92.2 +/- 1.8 and 98.4 +/- 2.4 mm Hg, respectively. Ramipril significantly affected the baroreceptor set point with a decrease in mean blood pressure (72.1 +/- 1.7 vs 76.4 +/- 0.9 mm Hg, p less than 0.01) in the presence of unchanged heart rate (71.7 +/- 0.9 vs 73.6 +/- 1.5 min-1). Baroreceptor sensitivity, estimated by the slope of the delta blood pressure versus delta heart rate relation, was not affected by ACE inhibition. Also, the pressor effect of exogenous norepinephrine was unchanged by converting enzyme inhibition. The present results show that ACE inhibition with ramipril in sodium-replete healthy volunteers induces a decrease in blood pressure that is not accompanied by changes in heart rate, pressor sensitivity to exogenous norepinephrine or baroreceptor sensitivity.

Adult↗