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Biomedical subjects

L Lind

Publications and source records attributed to L Lind.

At least 91 records · Page 5Linked to original sources
PubMed1999

Perianal streptococcal dermatitis. The possible protective role of alpha-streptococci against spread and recurrence of group A streptococcal throat infection.

OBJECTIVE: To follow the spread of beta-haemolytic streptococci group A (GAS) within a family and examine the protective activity of normally occurring alpha-streptococci against GAS tonsillitis. DESIGN: Follow up of recurrent GAS throat infection within a family. SETTING: Intra familial spread of GAS. PATIENTS: A family of four, the mother suffering from recurrent streptococcal tonsillitis and a son with perianal streptococcal dermatitis. RESULTS: The strain of the GAS found in the perianal region of the boy was identical with that found in the throat of his mother. She had recurrent streptococcal tonsillitis, while the boy remained healthy in the throat. She lacked interfering alpha-streptococci in the throat, while the boy had a massive growth of alpha-streptococci in his throat with capacity to inhibit the growth of the streptococcal isolate. MAIN OUTCOME MEASURES: Infection with GAS within a family correlated with the growth-inhibiting activity of the alpha-streptococci in vitro. CONCLUSIONS: The study demonstrated the spread of GAS from a patient with streptococcal dermatitis to the throat of another person within the family, and the hindrance of induction of infection in patients carrying interfering alpha-streptococci.

Anus Diseases↗
PubMed1999

Endothelium-dependent vasodilatation in treated and untreated hypertensive subjects.

It has repeatedly been shown that endothelium-dependent vasodilatation (EDV) is impaired in patients with untreated hypertension. The effect of antihypertensive treatment on EDV has, however, not been extensively investigated. In the present study, EDV and endothelium-independent vasodilatation (EIDV) were studied in 20 untreated and 41 treated hypertensive subjects and in 26 matched, normotensive controls by means of infusion of methacholine (MCh), 2 and 4 microg/min, evaluating EDV, and nitroprusside (SNP), 5 and 10 microg/min, evaluating EIDV, in the brachial artery. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. The vasodilatory action of MCh was impaired in untreated hypertensives compared with controls, with the response in the treated hypertensives in between the other two groups (p < 0.01 vs both of the other groups). EIDV, on the other hand, was enhanced in the treated hypertensives (p < 0.01), so that the MCh to SNP FBF ratio, an index of endothelial function, was attenuated in both treated and untreated hypertensives (0.97 +/- 0.24 and 0.96 +/- 0.15, respectively), compared with controls (1.27 +/- 0.29, p < 0.001). Both EDV and EIDV declined with increasing number of antihypertensive drugs used in the treated hypertensives (p < 0.05). In conclusion, the endothelial function index was found to be similarly depressed in both treated and untreated hypertensive subjects compared with normotensive controls. Antihypertensive therapy seems to improve the vasodilatory capacity in general rather than enhancing endothelial function.

Analysis of Variance↗
PubMed1999

Unusual, high genetic diversity of Aleutian mink disease virus.

The genetic diversity of Aleutian mink disease virus (AMDV) was examined. Sequences obtained from 35 clinical samples were compared with five published sequences. An unusual, high genetic variability was revealed. Three phylogenetic subgroups of AMDV were identified, and the presence of more than one genotype at some farms was detected.

Aleutian Mink Disease↗
PubMed1999

Impaired systolic and diastolic function and ventricular arrhythmia are common in normotensive healthy elderly men with left ventricular hypertrophy.

BACKGROUND: The present study was designed to assess the impact of left ventricular hypertrophy (LVH) independent of hypertension on the presence of silent myocardial ischemia and arrhythmia, as well as on systolic and diastolic function in otherwise healthy elderly men. METHODS AND RESULTS: Twenty apparently healthy normotensive subjects with LVH were compared with 18 hypertensive subjects with LVH and with 20 healthy subjects without LVH (controls)--all recruited from a health screening programme of 70-year-old men. All participants were free from known coronary heart disease and were evaluated by means of echocardiography with Doppler, a symptom-limited exercise test and 24 h ambulatory ECG monitoring. The healthy normotensive subjects with LVH showed impaired systolic function (ejection fraction 66 +/- 8 (SD)% versus 72 +/- 8% in controls, P < 0.03) and impaired diastolic function (E/A ratio 0.86 +/- 0.20 versus 1.12 +/- 0.30, P < 0.01) as well as an increased number of premature ventricular complexes in the exercise test and during the 24 h ECG monitoring (P < 0.05), when compared with the healthy group without LVH. The hypertensive subjects with LVH showed impaired diastolic function (P < 0.05) and a more pronounced ST depression in the exercise test (P < 0.05), when compared with the healthy group without LVH. In both of the LVH groups, more than 20% of the subjects evidenced ST-segment depression > or = 1 mm in the exercise test, compared with 5% of the healthy group without LVH. CONCLUSIONS: In elderly men free from hypertension or other known disease, LVH at echocardiography was associated with impaired systolic and diastolic function as well as with ventricular arrhythmia. Thus, even in the absence of hypertension, LVH may be a harmful characteristic in the elderly.

Aged↗
PubMed1999

Local vasodilatation with metacholine, but not with nitroprusside, increases forearm glucose uptake.

Insulin is known to increase blood flow in parallel to glucose uptake in skeletal muscle. However, it is not known if an increase in blood flow by itself is associated with an increase in glucose uptake in the absence of hyperinsulinemia. To investigate further this matter, the effect of increased blood flow on forearm glucose uptake was studied in the fasting state during intra-arterial infusions of two different vasodilators, metacholine and nitroprusside, in 19 hypertensive subjects. Both metacholine (4 microg/min) and nitroprusside (10 microg/min) increased resting forearm blood flow, measured by venous occlusion plethysmography, to a similar degree (180 % and 170 %, respectively, p<0.0001 for both). However, metacholine infusion increased the forearm glucose uptake from 2.0+/-0.9 (S.D.) during rest to 5.5+/-3.0 umol/min/100 ml tissue (p<0.0001), while no significant change in glucose uptake was seen during nitroprusside infusion (2.3+/-1.4 micromol/min/100 ml tissue). In conclusion, vasodilatation induced by metacholine, but not by nitroprusside, increased glucose uptake in the forearm of hypertensive patients. Thus, an increase in forearm blood flow does not necessarily improve glucose uptake in the forearm during the fasting state.

Adult↗
PubMed1998

[Left ventricular hypertrophy--an important, often unrecognized risk factor].

Epidemiological studies both in the general population and in series of hypertensive patients have shown the presence of left ventricular hypertrophy (LVH), as determined by echocardiography, to be a powerful risk factor for cardiovascular events. Although LVH is generally associated with hypertension, less than half of hypertensive patients develop LVH. Insulin resistance, endothelial dysfunction, increased blood viscosity, decreased arterial compliance, and increased angiotensin-converting enzyme activity have all been associated with the development of LVH. Although findings in observational studies suggest LVH regression to have a beneficial effect in terms of decreased cardiovascular risk, confirmation of this awaits the results of prospective clinical trials currently being carried out.

Humans↗
PubMed1998

The effect of euglucaemic hyperinsulinaemia on forearm blood flow and glucose uptake in the human forearm.

Insulin-mediated stimulation of blood flow to skeletal muscle has been proposed to be of major importance for insulin-mediated glucose uptake. The aim of this study was to investigate the relative importance of blood flow and glucose extraction as determinants of insulin-mediated glucose uptake in the human forearm. Forearm blood flow (FBF), glucose extraction and oxygen consumption were evaluated for 100 min during the euglycaemic hyperinsulinaemic clamp (92 mU/l) in nine healthy subjects. FBF was measured by venous occlusion plethysmography. Forearm glucose uptake increased sevenfold during the hyperinsulinaemia (P<0.001). Forearm glucose extraction showed a minor increase during the first 10 min of hyperinsulinaemia, but the most marked increase took place between 10 and 20 min (+170%). Thereafter, only a minor further increase was seen. During the first 10 min of hyperinsulinaemia FBF was unchanged. Thereafter, FBF increased steadily to a plateau reached after 60 min (+50%, P<0.001). A close relationship between whole body glucose uptake and FBF was seen at the end of the clamp (r = 0.75, P<0.02), but at this time the relationship between whole body glucose uptake and forearm glucose extraction was not significant. The modest increase in O2 consumption seen at the beginning of the clamp (+19%) was not related to FBF during the early phase of the clamp. In conclusion, the early course of insulin-mediated glucose uptake in the human forearm was mainly due to an increase in glucose extraction. However, with time the insulin-mediated increase in blood flow increased in importance and after 100 min of hyperinsulinaemia FBF was the major determinant of glucose uptake.

Adult↗
PubMed1998

Insulin resistance in essential hypertension is related to plasma renin activity.

A high plasma renin activity (PRA) has previously been related to several cardiovascular risk factors as well as to later cardiovascular events. As insulin resistance has been suggested as the unifying factor in the insulin resistance metabolic syndrome, insulin resistance was evaluated by the euglycaemic hyperinsulinaemic clamp technique in 50 untreated hypertensive subjects in whom PRA and serum aldosterone were measured together with lipids and an intravenous glucose tolerance test (IVGTT). PRA was inversely related to insulin-mediated glucose disposal during the clamp (r=-0.31, P < 0.05), as well as to fasting insulin (r=0.32, P < 0.05) and to insulin at 60 min at the IVGTT (r=0.30, P < 0.05), but not to other risk factors. Serum aldosterone was not related to any of the metabolic risk factors. In conclusion, the present investigation showed that insulin resistance is associated with elevated levels of PRA in patients with untreated essential hypertension. It thus seems as if a high activity in the renin system should be included in the disturbances included in the insulin resistance metabolic syndrome, a syndrome with a major impact on future cardiovascular events.

Aged↗
PubMed1998

Captopril, but not nifedipine, improves endothelium-dependent vasodilation in hypertensive patients.

The present study aimed to investigate the influence of the angiotensin-converting enzyme (ACE)-inhibitor captopril and the Ca-antagonist nifedipine on endothelium-dependent vasodilation (EDV) in the forearm of hypertensive patients. Twenty-three middle-aged untreated hypertensive patients underwent evaluation of EDV and endothelium-independent vasodilation (EIDV) in the forearm, by means of local intra-arterial infusions of methacholine (MCh, evaluating EDV) and sodium-nitroprusside (SNP, evaluating EIDV), before and 1 h after intake of either captopril (25 mg) or nifedipine (10 mg) in a randomised, double-blind fashion. A matched normotensive control group was investigated at baseline conditions only. Five of the hypertensives were also evaluated after 3 months of treatment with captopril 25 mg twice daily in an open pilot study. First, the vasodilation induced by methacholine (MCh), but not SNP, was significantly attenuated in the hypertensive patients compared to the normotensive controls (P < 0.001 at MCh 4 microg/min). Second, although the two drugs induced a similar decline in blood pressure (BP) 1 h after administration (-11 to 10 mm Hg/-8 to 7 mm Hg), captopril significantly potentiated the vasodilator response to MCh (+32+/-13%, MCh 4 micr og/min, P < 0.01) but not SNP, while nifedipine did not significantly alter the response to either MCh or SNP. The improvement in vasodilator response to MCh induced by captopril was closely related to the reduction in BP (r = 0.72, P < 0.01). Third, in the pilot study, 3 months of captopril treatment induced a significant potentiation of the vasodilator response to MCh (+34+/-17%, MCh 4 microg/min, P < 0.05) in parallel with a significant BP reduction (-22+/-24/13+/-13 mm Hg, P < 0.05), while the response to SNP was unchanged. In conclusion, the present study confirmed that essential hypertension is associated with a defect in EDV. Furthermore, an improvement in EDV was seen in hypertensive patients shortly after administration of captopril, but not nifedipine. In addition, a significant beneficial effect on EDV was seen in a small pilot study during long-term treatment with captopril.

Aged↗
PubMed1998

Acute hypertension impairs endothelium-dependent vasodilation.

1. Previous investigations have demonstrated an impaired endothelium-dependent vasodilatation (EDV) in patients with hypertension. The present study aimed to investigate if an acute rise in blood pressure to hypertensive levels impairs EDV in otherwise normotensive subjects. 2. Twenty-seven young, healthy, normotensive subjects were studied. Eight of these underwent evaluation of EDV and endothelium-independent vasodilatation (EIDV) by means of forearm blood flow measurements during local intra-arterial infusions of methacholine (2 and 4 micrograms/min) and sodium nitroprusside (5 and 10 micrograms/min), before and after 1 h of sustained hypertension, induced by noradrenaline given intravenously. Identical measurements were made in 11 subjects before and during concomitant local intra-arterial infusion of noradrenaline without change in blood pressure and eight subjects were studied during saline infusions. 3. One hour of sustained hypertension (diastolic blood pressure > 95 mmHg) significantly attenuated both forearm blood flow (17.4 +/- 6.8 versus 27.4 +/- 6.8 ml.min-1.100 ml-1 tissue at baseline, P < 0.05) and forearm vascular resistance decrease (3.2 +/- 0.87 versus 7.4 +/- 2.5 units at baseline, P < 0.05) during methacholine infusion. These attenuations were significantly more pronounced for methacholine than for sodium nitroprusside (P < 0.05). In contrast, local intra-arterial noradrenaline infusions impaired vasodilatation induced by methacholine and sodium nitroprusside to a similar extent. Saline infusions did not change either EDV or EIDV. 4. Thus, an acute rise in blood pressure to hypertensive levels induced by noradrenaline impaired EDV more than EIDV in otherwise normotensive subjects, while no such selective effect of local noradrenaline was seen, suggesting that a high blood pressure impairs endothelial vasodilator function.

Acute Disease↗
PubMed1998

Effects of endothelin receptor type A antagonism and nitric oxide synthase inhibition on cerebral blood flow in hypertensive rats.

Effects of the endothelin receptor type A antagonist BQ 123 and the NO synthase inhibitor L-NMMA on cerebral blood flow were studied in vivo in anaesthetized hypertensive (SHR) and normotensive (WKY) rats. The effects of acetylcholine following pre-treatment with these drugs were also studied with the microsphere method for blood flow determination in the cortex, thalamus, caudatus, pons, medulla, cerebellum and hypophysis. BQ 123 (1 mg kg-1) induced only minor effects on cerebral blood flow in both strains (n = 8), whereas L-NMMA (N = 8; 20 mg kg-1) reduced regional cerebral blood flow significantly in most regions (21-54%) in the hypertensive, but not in the normotensive rat. In normotensive rats pre-treated with BQ 123 intravenous administration of acetylcholine (2 micrograms kg-1 min-1) induced a widespread significant increase (20-50%) in cerebral blood flow despite a reduction of the mean arterial blood pressure, while no significant effects were seen in hypertensive animals. Intravenous infusion of acetylcholine in animals pre-treated with L-NMMA did not affect cerebral blood flow in most regions in either of the two rat strains. In conclusion, a vasodilatory response to acetylcholine was found following endothelin receptor A antagonism in the WKY rat only, suggesting a role for endothelin in the control of cerebral blood flow in this strain. Furthermore, a higher basal vasodilating nitric oxide-tone seems to be present in the hypertensive rat compared with the normotensive rat.

Acetylcholine↗
PubMed1998

Methodological aspects of the evaluation of endothelium-dependent vasodilatation in the human forearm.

The present study, involving 56 healthy subjects from a health screening, was undertaken to address some methodological questions regarding the measurement of endothelial function using local intra-arterial infusions of metacholine (2 and 5 micrograms min-1) to evaluate endothelium-dependent vasodilatation, and sodium nitroprusside (SNP, 5 and 10 micrograms min-1) to evaluate endothelium-independent vasodilatation. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. The ratio of FBF during the highest dose of metacholine to FBF during the highest dose of SNP was used as an index of endothelial function. In 10 young volunteers the procedure was repeated after 2 h and again after 3 weeks in order to study short-term and long-term reproducibility of the method. Neither the vasodilatatory response to metacholine (r = 0.006) nor that to SNP (r = 0.08) was related to resting FBF. Neither the circumference nor the length of the arm was related to endothelial function (r = 0.01-0.11), as evaluated by the FBF on metacholine to nitroprusside ratio (mean 1.3 +/- 0.3 SD). The use of a wrist cuff to exclude hand circulation, or not, did not influence the evaluation of endothelial function significantly. Maximal FBF after 3 min of arterial occlusion of the forearm was significantly related to blood flow during both metacholine (r = 0.53, P < 0.01) and nitroprusside infusion (r = 0.36, P < 0.05), but not to the FBF on metacholine to nitroprusside ratio (r = 0.01). The short-term and long-term reproducibility of FBF during vasodilatation with metacholine and SNP was good (r = 0.89-0.97, P < 0.001), while the individual measurements for resting FBF were less reproducible when repeated after 3 weeks (r = 0.34). In conclusion, endothelial function was not related to resting FBF, nor to the arm circumference or length. No major difference was seen whether endothelial function was evaluated with or without exclusion of the hand circulation. Maximal FBF during reactive hyperaemia was not related to endothelial function.

Adult↗
PubMed1998

Left ventricular geometry and function are related to electrocardiographic characteristics and diagnoses.

We investigated the relationships between echocardiographic indices of left ventricular geometry and function and major electrocardiographic (ECG) abnormalities in 540 elderly (69-74 years old) male participants of a health survey conducted in Uppsala county, Sweden. Comparing men with major ECG abnormalities that were present or absent in various hierarchic mutually exclusive categories, left ventricular mass indexed to body surface area (LVMI) was significantly increased with major Q-waves (P = 0.0002), ST or T-wave abnormalities (P = 0.005), left bundle-branch block (P = 0.005) and also with atrioventricular block type 1 (P = 0.008) and frequent premature beats (P = 0.02). The left atrial diameter was also significantly increased with most ECG abnormalities. The increased LVMI was in left bundle-branch block mainly due to an increased left ventricular diameter, whereas left ventricular wall thickness was increased with frequent premature beats, atrioventricular block type 1 and ST or T-wave abnormalities. The prevalence of Q-waves was highest in eccentric left ventricular hypertrophy, whereas the prevalence of ST or T-wave abnormalities and atrioventricular block type 1 was highest in concentric left ventricular hypertrophy. Both left ventricular systolic (ejection fraction) and diastolic function (E/A) ratio) were inversely related to Sokolow-Lyon QRS amplitude (r = -0.25, P < 0.02 and r = -0.22, P < 0.03 respectively). In conclusion, LVMI was increased in subjects with ECG signs of coronary artery disease as well as in subjects with several other ECG diagnoses. Furthermore, both left ventricular systolic and diastolic dysfunction were related to increased QRS amplitudes. Thus, the finding of ECG abnormalities in elderly men should raise the suspicion of structural and/or functional left ventricular abnormality.

Adult↗
PubMed1998

Parathyroid hormone and ionized calcium levels are related to the severity of illness and survival in critically ill patients.

BACKGROUND: The present study explores serum parathyroid hormone (PTH) and blood ionized calcium (Ca2+) levels in relation to the severity of disease and mortality in the intensive care unit (ICU). METHODS: In a pilot study, 37 consecutive critically ill patients admitted to the ICU were studied with determinations of serum PTH and total serum calcium within the first 24 h. In a following prospective study, patients suffering from sepsis (n = 13) or subjected to major surgery (n = 13) were investigated daily for 1 week with determinations of serum PTH and ionized calcium (Ca2+). Severity of disease was assessed by the APACHE II score and hospital mortality was recorded. RESULTS: In the pilot study, serum PTH levels were elevated (> 55 ng L-1) in 38% of the patients and were not related to serum calcium but showed a significant relationship to the APACHE II score (r = 0.39, P < 0.05). In the prospective study, serum PTH was elevated in 69% of the patients in both groups at inclusion, and 6 days later 87% of the septic and 37% of the surgery patients still showed elevated levels. Hypocalcaemia was more commonly seen in the septic patients [mean Ca2+ 1.03 +/- 0.08 (SD) mmol L-1] than in the surgical patients (1.14 +/- 0.06 mmol L-1) at inclusion. Both PTH and Ca2+ levels were significantly related to the APACHE II score (r = 0.46, P < 0.03, and r = -0.54, P < 0.009, respectively). Furthermore, PTH levels were significantly increased in non-survivors (n = 5) compared with survivors (mean 161 +/- 51 vs. 79 +/- 51 ng L-1, P < 0.005). CONCLUSION: Hypocalcaemia and increased levels of PTH were common findings in critically ill patients. These alterations in calcium homeostasis were related to the severity of disease and increased PTH levels were associated with a poor outcome.

APACHE↗
PubMed1998

Endothelium-dependent vasodilation in the uvea of hypertensive and normotensive rats.

PURPOSE: The effects of endothelium-related substances such as acetylcholine, a stimulator of endogenous NO-production, the NO-synthesis inhibitor L-NMMA, the exogenous NO-donor sodium nitroprusside and the endothelin (ET)A-receptor antagonist BQ123, on uveal blood flow were investigated in normotensive and hypertensive SHR rats. METHOD: The radioactively-labelled microsphere method was applied for the measurement of regional blood flow in the uvea. RESULTS: Under resting conditions, local blood flow was lower in the hypertensive animals. The increase in choroidal blood flow (145 +/- 50%; P < 0.01) and reduction in vascular resistance (-58 +/- 7%; P < 0.01) observed in the WKY after i.v. infusion of acetylcholine, 2 micrograms x kg bw-1 x min-1, were significantly less pronounced in animals pretreated with L-NMMA, indicating local formation of NO as a vasodilator mechanism. In contrast, acetylcholine did not induce significant vasodilation in the choroid of SHR rats. In the anterior uvea of both strains, acetylcholine did not affect local blood flow. L-NMMA, 20 mg x kg bw-1, alone reduced blood flow in the entire uvea of both strains. Intravenous injection of BQ123, 1 mg x kg bw-1, did not affect regional blood flow in the uvea of WKY or SHR animals. Infusion of acetylcholine following ETA-receptor blockade induced vasodilation in both the choroid and anterior uvea in the WKY but not in the SHR. CONCLUSIONS: Acetylcholine-stimulated NO-mediated vasodilation, but not basal NO-formation, was impaired in the choroid of the SHR. Furthermore, an interaction between vasoconstricting ET and acetylcholine was found in the anterior uvea of normotensive but not hypertensive rats.

Acetylcholine↗
PubMed1998

Divergent effects of different antihypertensive drugs on endothelium-dependent vasodilation in the human forearm.

Several studies indicated an abnormal endothelium-dependent vasodilation (EDV) in hypertensive patients, but no study has systematically investigated the effects of different pharmacologic classes of antihypertensive drugs on EDV. This study aimed to evaluate the effects of three different antihypertensive regimens [angiotensin-converting enzyme (ACE) inhibition, calcium channel blockade, and beta-blockade] on EDV when given locally in the forearm at a constant blood pressure. The increase in forearm blood flow (FBF) during local intraarterial infusions of methacholine (MCh; inducing EDV) and sodium nitroprusside (SNP; inducing endothelium-independent vasodilation, EIDV) was measured in young, normotensive subjects by venous occlusion plethysmography, before and during concomitant local intraarterial infusion of any of the antihypertensive drugs. Without changing baseline FBF, enalaprilat (n=6, 2.4 mg/h) potentiated the increase in FBF induced by MCh [from 22.6+/-2.3 (SD) to 25.4+/-2.3 ml/min/100 ml tissue at 4 microg/min; p < 0.05], but the response to SNP was unchanged. Local intraarterial verapamil infusion (n=6), at a dose individually titrated to keep baseline FBF unchanged, did not alter the response to MCh infusion, whereas the response to SNP was potentiated. A higher dose of verapamil (n=6), which increased baseline FBF, increased both EDV and EIDV significantly in parallel (p < 0.05). The local propranolol infusion (n=6, 1.2 mg/h) attenuated the FBF response to MCh significantly (from 28.9+/-5.7 to 21.5+/-3.2 ml/min/100 ml tissue at 4 microg/min; p < 0.05), whereas both baseline FBF and the response to SNP were unchanged. In conclusion, this investigation showed that commonly used antihypertensive drugs affect endothelial vasodilator function in a different ways. ACE inhibition enhanced EDV, whereas a nonselective beta-blocker attenuated EDV. The calcium channel blocker, verapamil, improved both EDV and EIDV, probably by a direct effect on the vascular smooth-muscle cells.

Antihypertensive Agents↗
PubMed1998

Effects of nitric oxide synthase inhibition and endothelin ETA receptor blockade on haemodynamics in hypertensive rats.

1. The objectives of the present study were to study regional differences in haemodynamics between spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats induced by the nitric oxide synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) and the endothelin ETA receptor antagonist BQ 123 in vivo in tissues known to be important for blood pressure (BP) regulation (heart, kidney and skeletal muscle). Furthermore, the effect of acetylcholine (ACh) infusion (2 micrograms/kg per min) was examined after L-NMMA or BQ 123. The microsphere method was used for determinations of cardiac index (CI) and regional haemodynamics. 2. NG-Monomethyl-L-arginine (20 mg/kg) increased BP (26-48%; P < 0.01) and reduced CI in both rat strains. BQ 123 (1 mg/kg) reduced BP slightly (-4 to 11%; P < 0.05). 3. NG-Monomethyl-L-arginine significantly increased myocardial and skeletal muscle vascular resistance in SHR only; however, in the kidney, L-NMMA reduced blood flow and increased vascular resistance in both rat strains. 4. BQ 123 induced minor changes in regional haemodynamics that were not significantly different between the two strains. 5. Acetylcholine following BQ 123 induced an increase in myocardial blood flow in WKY rats, but decreased blood flow in SHR. Acetylcholine following L-NMMA reduced myocardial blood flow in both strains. 6. Acetylcholine following BQ 123 induced renal vasodilation in WKY rats but, following L-NMMA, ACh did not induce renal vasodilation in either rat strain. In contrast, L-NMMA did not abolish the vasodilation of acetylcholine in skeletal muscle in WKY rats. 7. In conclusion, the contribution of nitric oxide to basal vessel tone was not impaired in the heart, skeletal muscle and kidney in SHR. Antagonism of ETA receptors caused similar haemodynamic responses in both rat strains in these organs. Furthermore, NOS inhibition, but not ETA blockade, blunted the expected ACh-induced vasodilation in the heart and kidney in WKY rats, but not in skeletal muscle in both strains.

Acetylcholine↗