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Biomedical subjects

W Kiowski

Publications and source records attributed to W Kiowski.

At least 91 records · Page 5Linked to original sources
PubMed1994

Aortic valve replacement in elderly patients with aortic stenosis.

OBJECTIVE: To assess the risk of aortic valve replacement and long-term follow-up in elderly patients with dominant aortic stenosis. DESIGN: Retrospective analysis of patients who had aortic valve replacement over a 10 year period and were routinely seen in an outpatient clinic. SETTING: University hospital. PATIENTS: 93 patients aged > or = 60 and 47 patients > or = 70 years with symptomatic aortic stenosis undergoing aortic valve replacement. MAIN OUTCOME MEASURES: Early and late mortality in different age groups. Influence of preoperative signs and symptoms on overall outcome. RESULTS: The proportion of patients older than 70 years increased from 11% in 1978 to 54% in 1986. Perioperative mortality was 3.6% and mortality after 2 and 5 years was 9% and 13% respectively. Survival was similar (85% and 83%, respectively) in patients aged 60-69 years (group 1, n = 93, mean age 64.5 (2.7) and patients aged > or = 70 years (group 2, n = 47, mean age 72.6 (2.5)). Additional coronary artery disease and coronary bypass grafting did not significantly affect survival. The cardiothoracic ratio was inversely related to survival (Cox regression, p < 0.05). Preoperative symptoms (syncope, angina pectoris, and dyspnoea) were similar in both patient groups. After a mean (SD) follow up of 51 (33) months 96% of surviving patients were in NYHA functional class I or II with no difference between the two age groups. Similarly, the cardiothoracic ratio and Sokolow index decreased to near normal values in both age groups. CONCLUSION: The risk of aortic valve replacement in patients with dominant aortic stenosis is low and not significantly influenced by age. Therefore replacement may be performed without increased risk in elderly patients and with a good long-term outcome.

Age Factors↗
PubMed1994

Diminished vascular response to inhibition of endothelium-derived nitric oxide and enhanced vasoconstriction to exogenously administered endothelin-1 in clinically healthy smokers.

BACKGROUND: Smoking is a major risk factor for the development of atherosclerosis. Because endothelial dysfunction may be a marker for future atherosclerosis, we investigated the effects of smoking on endothelium-dependent control of vascular tone. METHODS AND RESULTS: The effects of brachial arterial infusions of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide synthesis inhibitor; sodium nitroprusside; endothelin-1; and norepinephrine on forearm blood flow (strain-gauge plethysmography) were compared in 29 long-term smokers and 16 nonsmokers. The acute effects of smoking on systemic hemodynamics, plasma catecholamines, and forearm vascular responses to these compounds were investigated in smokers only. Smokers did not differ from nonsmokers (n = 16) regarding the vascular effects of sodium nitroprusside (n = 13) or vasoconstriction due to norepinephrine and endothelin-1 (n = 16). Low-dose endothelin-1-induced vasodilation, believed to reflect endothelial prostacyclin or nitric oxide release, was absent in smokers (n = 16), and their increase of forearm vascular resistance (FVR) after L-NMMA (n = 13) was impaired (35.6 +/- 27.9% versus 118.8 +/- 43.2%, P < .001). Short-term smoking (n = 11) increased blood pressure, heart rate, and plasma epinephrine concentrations (P < .05 or less); enhanced endothelin-1-induced vasoconstriction (delta FVR, 457 +/- 192% versus 254 +/- 143%, P < .01); and decreased norepinephrine-induced vasoconstriction (P < .05), but had no effect on the other interventions. CONCLUSIONS: Long-term smoking is associated with a diminished nitric oxide-dependent component of basal vascular tone and an impaired endothelium-dependent vasodilator response to low-dose endothelin-1 and short-term smoking enhances endothelin-1-induced vasoconstriction. Impaired endothelial control of vascular tone might reflect impairment of normal antiatherosclerotic endothelial functions in smokers, but the relevance of smoking-induced enhancement of endothelin-1 vasoconstriction remains to be determined.

Adult↗
PubMed1994

Angiotensinergic versus nonangiotensinergic hemodynamic effects of converting enzyme inhibition in patients with chronic heart failure. Assessment by acute renin and converting enzyme inhibition.

BACKGROUND: The contribution of nonangiotensinergic effects of converting enzyme inhibitors to their hemodynamic effects in patients with chronic heart failure is not clear. A comparison of the effects of renin and converting enzyme inhibition should help to clarify this issue. METHODS AND RESULTS: Thirty-six patients with chronic heart failure (New York Heart Association class II or III) were randomly assigned to receive double-blind either intravenous placebo, the renin inhibitor remikiren, or the converting enzyme inhibitor enalaprilat followed by coinfusion of a second placebo infusion, the addition of remikiren to enalaprilat, or the addition of enalaprilat to remikiren, respectively. Systemic hemodynamics (Swan-Ganz and radial artery catheters) were measured before (rest and submaximal recumbent bicycle ergometry), during (rest), and at the end (rest and exercise) of each 45-minute single- or combination-infusion period. Placebo did not change hemodynamics or renin activity. Effective inhibition of the renin-angiotensin system by remikiren and enalaprilat was indicated by increases of plasma immunoreactive renin together with rapid and complete inhibition of renin activity after remikiren and an increase after enalaprilat (all P < or = .05). Remikiren and enalaprilat rapidly and to a similar extent reduced resting blood pressure through a reduction of systemic vascular resistance, and these changes were significantly correlated to baseline plasma renin activity. Both compounds also decreased pulmonary artery, pulmonary capillary wedge, and right atrial pressures to a similar extent (P < .05). During exercise, pulmonary capillary wedge and right atrial pressures were equally reduced and stroke volume index was increased with remikiren and enalaprilat (P < .05) for both). The combination of converting enzyme with renin inhibition or vice versa did not cause additional hemodynamic changes. CONCLUSIONS: Specific renin inhibition in patients with chronic heart failure produces short-term hemodynamic effects that are almost indistinguishable from those of converting enzyme inhibition. This finding and the lack of additional effects of converting enzyme inhibition added to renin inhibition suggest that nonangiotensinergic effects of converting enzyme inhibitors do not play a significant role in their short-term hemodynamic effects in patients with chronic heart failure.

Adult↗
PubMed1994

Vascular effects of endothelin-1 in humans and influence of calcium channel blockade.

AIM: To investigate the effects of brachial artery infusions of endothelin-1 on forearm blood flow in normal healthy volunteers. METHODS: Brachial artery cannulation was used for a direct assessment of blood pressure and for intra-arterial regional drug infusions. Drug-induced forearm blood flow changes were measured by venous occlusion plethysmography. RESULTS: Low-dose endothelin-1 infusions resulted in a significant increase in forearm blood flow, indicating vasodilation, which was significantly attenuated by cyclo-oxygenase inhibition using aspirin. High-dose endothelin-1 infusions resulted in transient vasodilation, followed by dose-dependent and long-lasting vasoconstriction. In the human forearm the vasoconstrictor potency of endothelin-1 was approximately 10-15 times greater than that of norepinephrine. Maximal cyclic GMP-dependent vascular muscle relaxation, after muscarinergic stimulation by acetylcholine (endothelium-dependent) or after infusion of sodium nitroprusside (endothelium-independent), did not prevent endothelin-1 induced vasoconstriction. However, calcium channel blockade by brachial artery infusions of maximally vasodilating doses of either verapamil or nifedipine not only abolished the endothelin-induced vasoconstriction but also unmasked the vasodilator potency of high-dose endothelin-1 infusions. The infusion of lower doses of nifedipine indicated that endothelin-1 induced vasoconstriction was reversed by plasma concentrations estimated to be in the therapeutic range. CONCLUSIONS: These results demonstrate a dual action of luminally applied endothelin-1 in human resistance vessels in vivo, consisting of transient initial vasodilation followed by pronounced vasoconstriction, and suggest that blockade of voltage-operated calcium channels can effectively counter the vasoconstrictor effects of endothelin-1.

Adult↗
PubMed1993

Silent ischemia after percutaneous transluminal coronary angioplasty: incidence and prognostic significance.

OBJECTIVES: The objective of this observational study was to assess the incidence and prognostic significance of silent ischemia after percutaneous transluminal coronary angioplasty. BACKGROUND: Apart from coronary angioplasty, prognosis of patients with silent ischemia is similar to that of patients with angina pectoris. However, similar data concerning silent ischemia associated with restenosis after coronary angioplasty are missing. METHODS: A consecutive series of 490 patients was investigated for asymptomatic ischemia on thallium-201 scintigraphy 6 months after successful coronary angioplasty. Repeat angiography was performed in a subgroup of patients with ischemia and repeat angioplasty was performed when clinically indicated. Patients were followed up for 2.2 +/- 0.8 years for cardiac events. RESULTS: Six months after coronary angioplasty, ischemia was present in 112 (28%) of 405 patients, and 60% of these 112 were asymptomatic. Ischemia was associated with significant stenosis in 97%; in contrast, results of exercise electrocardiography were negative in 74% of patients with scintigraphic ischemia and angiographic restenosis. The degree of restenosis was similar in patients with symptomatic or silent ischemia (80 +/- 16% vs. 81 +/- 21%). The long-term prognosis of patients with silent ischemia was remarkably similar to that of symptomatic patients. A worse outcome of symptomatic patients was found only if repeat coronary angioplasty for restenosis was considered a separate event (p < 0.01). Silent and symptomatic ischemia predicted an increased risk for recurrent ischemic events but not for death. CONCLUSIONS: Thus, absence of symptoms and negative findings on an exercise electrocardiogram may not reflect a good angioplasty result. In addition, silent ischemia due to restenosis after coronary angioplasty has a significant prognostic importance for recurrent symptomatic ischemic events that may be reduced by repeat angioplasty.

Aged↗
PubMed1993

[Long-term effect of amiodarone therapy following myocardial infarct in patients with complex ventricular arrhythmias].

In the BASIS study, an improvement in 1 year survival of patients with asymptomatic complex ventricular arrhythmias with low-dose amiodarone was shown in comparison with an untreated control group. To assess whether this beneficial effect would last for a longer follow-up despite discontinuation of amiodarone therapy after one year, we assessed long-term survival and mode of death in the 91 survivors of the first year in the amiodarone treatment group and the 99 survivors in the control group by phone calls to private physicians, patients and hospitals. During a median follow-up of 72 (55-125) months, 184/193 patients (95%) could be reached. Causes of death during the follow-up were sudden (6 vs 14), non-sudden cardiac (8 vs 9), non cardiac (5 vs 9) and unknown (7 vs 6) in patients initially treated with amiodarone versus the control group respectively. The probability of death after 84 months was 30% in the amiodarone group and 45% in the control group, and was significantly lower in amiodarone treated patients with respect to all deaths (p = 0.024) as well as cardiac deaths (p = 0.027). This mortality reduction was only due to amiodarone treatment during the first year after the index infarction, whereas the survival curves did not differ significantly during the late follow-up. Thus, the risk of cardiac death is low after the first year after myocardial infarction and may not justify continued antiarrhythmic therapy in patients with initially complex asymptomatic ventricular arrhythmias.

Aged↗
PubMed1993

Effects of angiotensin converting enzyme inhibition on endothelial vasodilator function in primary human hypertension.

Hypertension in animal models and in humans is associated with a decreased vasodilator response to acetylcholine which causes vascular relaxation by release of endothelium-derived relaxing factor from the endothelium. Since lowering of blood pressure, particularly with angiotensin converting enzyme inhibitors, improved the response to acetylcholine we investigated the effects of brachial artery infusions of ascending dosages of acetylcholine on forearm blood flow before and after 5 months of therapy with the angiotensin converting enzyme inhibitor, cilazapril, in 10 patients with mild to moderate primary hypertension. Cilazapril decreased blood pressure from 150.8 +/- 14.4/98.9 +/- 4.3 mmHg during placebo to 138.8 +/- 15.6/88.6 +/- 8.9 mmHg (P < 0.01). Brachial artery acetylcholine infusions increased forearm blood flow from 2.95 +/- 1.5 to a maximum of 22.8 +/- 11.5 ml.min-1.100 ml-1 forearm tissue and decreased forearm vascular resistance from 48.1 +/- 34.1 to 6.9 +/- 6.9 units before cilazapril. This response did not change after cilazapril therapy. Our findings in patients with primary hypertension, therefore, do not support the concept that angiotensin converting enzyme inhibition influences endothelium-dependent vascular relaxation to acetylcholine to a significant degree. Whether this lack of effect on endothelial vasodilator function is specific for the vascular bed chosen for study or whether it represents a fundamental difference between animal models and human hypertension remains an important issue to be clarified.

Acetylcholine↗
PubMed1993

Circadian variation of ischemic cardiac events.

Analysis of the circadian distributions of silent ischemic episodes and myocardial infarction has revealed a circadian variability with peak event incidences in the morning hours after awakening. This morning peak of ischemic events is paralleled by circadian variations of blood pressure and heart rate that reflect an increase of sympathetic activity. The increase in blood pressure and heart rate is accompanied by a morning increase of platelet aggregability and a decrease in endogenous fibrinolytic activity. The increase in sympathetic activity may lead to inadequate vasoconstriction in atherosclerotic coronary arteries, which, in combination with mechanical factors such as elevated blood pressure, may lead to plaque rupture. The enhanced thrombogenicity of the blood might facilitate or accelerate thrombus formation and can help to explain the circadian variability of myocardial infarctions caused by occlusive coronary thrombi. Further characterization of the underlying mechanisms of the circadian variability might ultimately lead to more effective prevention, especially during the vulnerable morning hours.

Blood Pressure↗
PubMed1993

Long-term benefit of 1-year amiodarone treatment for persistent complex ventricular arrhythmias after myocardial infarction.

BACKGROUND: In the Basel Antiarrhythmic Study of Infarct Survival trial, low-dose amiodarone improved 1-year survival in patients with asymptomatic complex ventricular arrhythmias persisting 2 weeks after myocardial infarction. To assess whether this beneficial effect persisted despite discontinuation of amiodarone after 1 year, the long-term outcomes of all patients of the amiodarone-treated group (initially n = 98) and those of the control group (n = 114) were assessed. METHODS AND RESULTS: After a mean follow-up of 72 (55-125) months, information on 96% of patients (203 of 212) was obtained regarding survival or cause of death. The probability of death after 84 months according to actuarial life-table analysis (Kaplan-Meier) was 30% for the amiodarone-treated patients and 45% for control patients. For the total follow-up, mortality remained significantly lower in the amiodarone group versus the control group regarding all deaths (p = 0.03) as well as cardiac death (p = 0.047). This mortality reduction was entirely due to the first-year amiodarone effect, since there was no significant mortality difference between groups when considering survival after discontinuation of amiodarone only. CONCLUSIONS: These data suggest that the beneficial effect of amiodarone on survival in this high-risk group of patients persists for several years. In addition, the results stress the importance of early treatment after myocardial infarction, whereas the rate of sudden death and all cardiac death is low (1.6% and 4.1% per year, respectively) during late follow-up and therefore may not warrant further therapy.

Amiodarone↗
PubMed1993

Atrial natriuretic peptide release and volume regulation following kidney transplantation.

The major stimulus for atrial natriuretic peptide (ANP) release is atrial stretch and increased values are observed in volume overload states such as chronic renal failure. Since successful kidney transplantation restores volume homeostasis, we compared the effects of human cadaveric kidney transplantation on time course and changes of plasma ANP in the early postoperative period in 4 patients with successful and 4 patients with failed transplantation. ANP concentrations were elevated before transplantation in both groups (91 +/- 16 and 70 +/- 32 pmol/l) and decreased after successful (50 +/- 27 pmol/l, day 16) but increased after failed transplantation (146 +/- 45 pmol/l, day 16). Moreover, there was a close correlation between changes of body weight and ANP concentrations. Plasma renin activity decreased and plasma noradrenaline increased non-significantly in both groups, the latter more so after failed transplantation (116 +/- 42 to 194 +/- 156 vs 156 +/- 157 to 425 +/- 287 ng/l). No correlation was found between changes of renin activity or plasma catecholamines and ANP concentrations. The results indicate that the mechanisms governing release of atrial natriuretic peptide are operative in patients with chronic end-stage renal failure and after successful kidney transplantation with a return of atrial natriuretic peptide concentrations towards normal in the latter.

Adult↗
PubMed1993

[Pathophysiology of heart failure: peripheral vascular and muscular mechanisms].

Exercise tolerance in patients with congestive heart failure correlates poorly with measures of systolic left-ventricular function and is determined by disturbances of the regulation of skeletal muscle perfusion and structural and metabolic changes of skeletal muscle itself. The increase in minimal vascular resistance in skeletal muscle is due to increased activities of the sympathetic nervous system, the renin-angiotensin and vasopressin systems and decreased and increased endothelium-mediated vasodilation and vasoconstriction, respectively. In addition, skeletal muscle atrophy, decreased oxidative capacity and a relative increase of easily fatiguable glycolytic muscle fibres also contribute to the reduction of exercise tolerance. The disturbances of skeletal muscle perfusion and changes of skeletal muscle are at least in part reversible by vasodilator therapy or, in the extreme situation, by cardiac transplantation.

Heart Failure↗
PubMed1992

[Ambulatory long-term blood pressure determination: technique and ways of risk identification].

Traditional noninvasive measurement of blood pressure with the sphygmomanometer has as a punctual method been considerably expanded by the development of methods for recording blood pressure repeatedly under normal daily activity. Such procedures have contributed much to understanding of circadian regulation of blood pressure. Normo- and hypertensive patients experience a physiologic drop in systolic and diastolic blood pressure during night hours. Ambulatory blood pressure recordings are suitable to increase treatment compliance by patients. They allow qualitative evaluation of antihypertensive treatments and elimination of overshooting reactions to the measuring process by the physician (white-coat effect). This method has the potential for better definition of cardiovascular risk factors through recording of circulatory stress by blood pressure. No accepted guidelines exist, however, to date for definition of normal values for such measurements. The upper limits of normality for averaged blood pressure appear to be 140/90 mmHg during the day and 120/80 mmHg at night.

Blood Pressure↗
PubMed1992

Beneficial effect of amiodarone on cardiac mortality in patients with asymptomatic complex ventricular arrhythmias after acute myocardial infarction and preserved but not impaired left ventricular function.

To determine whether the beneficial effect of low-dose amiodarone on survival in patients with complex ventricular arrhythmias after myocardial infarction was dependent on left ventricular (LV) function, results of the Basel Antiarrhythmic Study of Infarct Survival were analyzed. Two hundred twelve patients after acute myocardial infarction with asymptomatic complex arrhythmias were randomly assigned to receive amiodarone 200 mg/day or to a control group and followed up for 1 year. Results of mortality and arrhythmic events were related to baseline radionuclide LV ejection fraction. With preserved (greater than or equal to 40%) LV ejection fraction, there was a significantly lower 1-year cardiac mortality in patients treated with amiodarone (1 of 68 or 1.5%) versus control subjects (5 of 56 or 8.9%; p less than 0.03). This was not the case for patients with LV ejection fraction less than 40%. Similarly, arrhythmic events were significantly reduced only in patients with preserved LV function. These results suggest an interaction between the effects of amiodarone on survival and LV dysfunction in patients after acute myocardial infarction. Because of 2 other small studies with similar results, this finding may be of clinical relevance and should be addressed in ongoing and future research with this drug.

Aged↗
PubMed1992

Reversal of endothelin-1-induced vasoconstriction by nifedipine in human resistance vessels in vivo in healthy subjects.

The influence of blockade of voltage-operated calcium channels by nifedipine on endothelin-1-induced vasoconstriction was investigated in 10 healthy volunteers. Brachial artery infusions of nifedipine (0.25, 0.5, 1 and 3 micrograms/min/100 ml forearm tissue) resulted in dose-dependent increases (mean +/- SD) in forearm blood flow (103 +/- 63% to 833 +/- 426%). Intraarterial infusions of endothelin-1 (50 ng/min/100 ml) resulted in transient increases in forearm blood flow (2.6 +/- 0.9 vs 3.9 +/- 2.0 ml/min/100 ml, p less than 0.01) in the first minute of infusion and subsequent decreases (to 1.0 +/- .5 ml/min/100 ml, p less than 0.01) in the third minute of infusion. Endothelin-1-induced vasoconstriction was reversed by the lowest dose of nifedipine, whereas the higher dosages of nifedipine further increased forearm blood flow to 12.5 +/- 6.4 ml/min/100 ml. The percent increase of forearm blood flow during co-infusion of endothelin-1 and the highest dosage of nifedipine was significantly greater compared with nifedipine alone (1,204 +/- 531% vs 833 +/- 426%, p less than 0.05). The results demonstrate a dual action of luminally applied endothelin-1 in human resistance vessels in vivo (e.g., transient initial vasodilation followed by pronounced vasoconstriction) and suggest that blockade of voltage-operated calcium channels can effectively counteract the vasoconstrictor effects of endothelin-1.

Adult↗
PubMed1992

[Endothelin-induced vasoconstriction in man: variable modification caused by endothelium-derived relaxing factor, Sodium nitroprusside and calcium antagonists].

The vascular effects of endothelin-1 (ET) were investigated in 25 healthy volunteers by measuring changes of forearm blood flow in response to brachial artery ET infusions. ET in a low dose (0.5 ng/min/100 ml tissue) resulted in a small but significant increase of forearm blood flow (FBF) from 2.3 +/- 1.5 to 2.5 +/- 1.5 ml/min/100 ml (n = 25, p less than 0.05) while higher dosages (25 and 50 ng/min/100 ml) resulted in significant decreases of FBF to 1.78 +/- 1.3 and 1.1 +/- 0.9 ml/min/100 ml (p less than 0.01). Neither sodium nitroprussid (n = 6) nor acetylcholine (n = 7) prevented ET-induced vasoconstriction. In contrast, both verapamil (n = 6) and nifedipine (n = 6) not only prevented ET-induced vasoconstriction but resulted in additional vasodilatation to values above those seen with the calcium antagonists alone. Thus, in human resistance vessels ET has a dual action with vasodilation occurring at low dosages and vasoconstriction at high dosages. Blockade of voltage-operated calcium channels prevents ET-induced vasoconstriction and unmasks the vasodilatory effects of high ET-dosages. Blockade of voltage-operated calcium channels but not cyclic GMP dependent vasodilation appears to be an effective tool in preventing ET-induced vasoconstriction.

Acetylcholine↗
PubMed1992

[Technique and interpretation of 24-hour blood pressure measurements].

Development of ambulatory repetitive recording of blood pressure during day and night under normal daily activity demonstrates a marked fall in blood pressure of normo- and hypertensive individuals during the night hours. Although no general consensus exists on normal values for such measurements, the upper normal limit appears to be 140/90 mmHg during the day and 120/80 mmHg during the night. This method also avoids the excessive rise in blood pressure induced by the physician (white-coat effect). Furthermore, it permits an exact assessment of efficacy of antihypertensive treatment. It may also provide means for better characterization of hypertension as risk factor in general, although there is still a lack of experience to estimate its cardio-vascular risk potency.

Antihypertensive Agents↗
PubMed1992

Blood pressure control by the renin-angiotensin system in normotensive subjects. Assessment by angiotensin converting enzyme and renin inhibition.

BACKGROUND: The participation of the renin-angiotensin system in the control of blood pressure in normal, sodium-replete subjects is not clear. The use of a specific inhibitor of human renin should allow a better delineation of the importance of this system. METHODS AND RESULTS: Blood pressure responses were measured 1 hour after randomized, double-blind administration of the renin inhibitor Ro 42-5892 (600 mg p.o.) or the angiotensin converting enzyme inhibitor captopril (50 mg p.o.) in 20 healthy men on an ad libitum sodium diet. Effective inhibition of the renin-angiotensin system by either compound was indicated by increases of immunoreactive renin associated with an increase of angiotensin I production rate of 67.8 +/- 33.6% after captopril and a decrease of 79.5 +/- 16.4% after Ro 42-5892. Furthermore, Ro 42-5892 decreased plasma renin activity by 64%. Whereas intra-arterial diastolic (60 +/- 5.1 to 51.4 +/- 7.2 mm Hg, p less than 0.01) and mean arterial (77.7 +/- 6.0 to 71.4 +/- 8.5 mm Hg, p less than 0.001) pressures decreased after captopril, they remained unchanged after Ro 42-5892. Captopril, but not Ro 42-5892, increased forearm blood flow (2.4 +/- 0.8 versus 1.9 +/- 0.8 ml/min/100 ml, p less than 0.01) and significantly enhanced the increase of forearm blood flow to brachial artery infusions of bradykinin (0.15, 1.5, 5, 15, and 50 ng/min/100 ml; 5 minutes each) from 744 +/- 632% to 1,383 +/- 514% (p less than 0.01). Furthermore, repeat bradykinin infusions resulted in further decreases of blood pressure (from mean pressure of 71.4 +/- 8.5 to 63.2 +/- 7.6 mm Hg, p less than 0.01) only after captopril. Changes of blood pressure after captopril were unrelated to baseline plasma renin activity but correlated with captopril-induced enhancement of vasodilation to bradykinin (r = 0.68, p less than 0.05). CONCLUSIONS: The lack of blood pressure effects of renin inhibition in contrast to angiotensin converting enzyme inhibition suggests that the renin-angiotensin system does not contribute significantly to blood pressure control in normotensive, sodium-replete subjects. The hypotensive activity of angiotensin converting enzyme inhibitors may result from additional hormonal effects, for example, inhibition of bradykinin degradation and/or subsequent increases of vasodilating prostaglandins or endothelium-derived relaxing factor(s).

Adult↗