The effect of captopril on the reflex control heart rate: possible mechanisms.

Aa, Ajayi; Campbell, BC; Modesti, Pietro Amedeo; Kelman, Andrew W.; Reid, JL

doi:10.1111/j.1365-2125.1985.tb02793.x

Cited by 56 publications

(19 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…21 They also show lack of reflex tachycardia 22 and cause inhibition of the normal tonic influence of Ang II on the sympathetic nervous system. 23 During ACE inhibition, heart rate responses to postural changes and exercise are not impaired. 24 …”

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

2009

View full text Add to dashboard Cite

Since their inception, angiotensin-converting enzyme (ACE) inhibitors have been used as first-line therapy for the treatment of cardiovascular and renal diseases. They restore the balance between the vasoconstrictive salt-retentive and hypertrophy-causing peptide angiotensin II (Ang II) and bradykinin, a vasodilatory and natriuretic peptide. As ACE is a promiscuous enzyme, ACE inhibitors alter the metabolism of a number of other vasoactive substances. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and promote natriuresis. They have been proven effective in the treatment of hypertension, and reduce mortality in congestive heart failure and left ventricular dysfunction after myocardial infarction. They inhibit ischemic events and stabilize plaques. Furthermore, they delay the progression of diabetic nephropathy and neuropathy and act as antioxidants. Ongoing studies have elucidated protective roles for them in both memory-related disorders and cancer. INTRODUCTIONIn recent years, stressful and fiercely competitive lifestyles and food habits have compounded the problems of hypertension. Long-standing and stressful, progressively rising hypertension can lead to many disorders, including myocardial infarction (MI), cerebrovascular events, congestive heart failure, peripheral arterial insufficiency, premature mortality 1 and renal dysfunction leading to glomerulosclerosis and kidney artery aneurysm. 2 A number of therapies are available, but angiotensin-converting enzyme (ACE) inhibitors have been the preferred first-line therapy for hypertension, congestive heart failure, left ventricular (LV) systolic dysfunction and MI. 3,4 ACE inhibitors (ACEis) have been in use for the past two decades, and the interest in them is still growing. Recently, the discovery of domain-selective ACEis and new members of the renin-angiotensin system (RAS) (that is, angiotensin-converting enzyme 2) have again fueled the interest of researchers. Some new studies have expanded the already impressive clinical profile of ACEis. This review traces some already known and new facets of ACE inhibition and introduces new advances in the designing of a new generation of ACEis.

show abstract

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

2009

View full text Add to dashboard Cite

show abstract

“…The absence of reflex tachycardia with blood pressure reduction after ACE inhibitors appears, in part, to be related to an enhancement of cardiac parasympathetic tone (Sturani et al, 1982;Campbell et al, 1985;Ajayi et al, 1985a) following the withdrawal of the vagolytic actions of angiotensin II (Ajayi et al, 1985b).…”

Section: Autonomic Function Testsmentioning

confidence: 99%

The pharmacodynamics and dose‐response relationships of the angiotensin converting enzyme inhibitor, cilazapril, in essential hypertension.

Aa¹,

Elliott²,

Reid³

1986

Brit J Clinical Pharma

Self Cite

View full text Add to dashboard Cite

In a double‐blind, placebo controlled, crossover study 12 patients with essential hypertension received single doses of 5, 10 and 20 mg of cilazapril, a new angiotensin converting enzyme (ACE) inhibitor. All doses similarly and significantly (P less than 0.05) reduced supine and erect blood pressure without increasing heart rate. The hypotensive effect was evident within 1 h, maintained for up to 8 h, with a maximal effect at 6 h. There was no discernible effect on blood pressure at 24 h after dosing. Plasma ACE activity was markedly inhibited to the same extent after all doses, with a peak inhibition of 94‐96% at 2‐3 h. At 24 h residual inhibition of ACE was 49‐54%. Plasma renin activity increased in a dose‐dependent manner with a peak at 6 h, and returned to baseline at 24 h. No correlation was found between the reduction in blood pressure and plasma renin activity, either at baseline or following cilazapril. There were no significant changes in plasma noradrenaline and the responses to upright posture and to dynamic exercise were preserved. There was no evidence of impaired exercise performance. Cilazapril is a potent ACE inhibitor with a rapid onset and a prolonged duration of action. These results suggest that peak ACE inhibition is achieved by 5 mg and that lower doses may be useful in clinical practice.

show abstract

“…The absence of reflex cardioacceleration, even after acute dosing, suggests that ACE inhibitors exert some specific influence on, for example, autonomic reflex mechanisms or baroreflex integrity. There is no evidence to suggest that ACE inhibition significantly modifies either sympathetic tone or baroreflex function in man (Millar et al, 1982) but enhancement of-cardiac parasympathetic activity has been reported with captopril, enalapril and lisinopril (Sturani et al, 1982;Campbell et al, 1985;Ajayi et al, 1985a, b …”

Section: Introductionmentioning

confidence: 99%

The influence of cilazapril on indices of autonomic function in normotensives and hypertensives.

Elliott

Reid

1989

Brit J Clinical Pharma

Self Cite

View full text Add to dashboard Cite

1. In two single dose studies, acute blood pressure reduction with cilazapril was not associated with any significant change in supine or erect heart rate in either normotensives or hypertensives. 2. To investigate the lack of reflex cardioacceleration, a series of autonomic function tests was undertaken when there was maximum ACE inhibition, maximum evidence of angiotensin II withdrawal and the lowest blood pressure. 3. There was no evidence that cilazapril had any significant impact on indices of sympathetic nervous activity or the integrity of baroreflex mechanisms. 4. The results for the bradycardic response to apnoeic facial immersion, suggested enhanced parasympathetic activity, consistent with the withdrawal of the vagolytic actions of angiotensin II. 5. These results suggest that the absence of a heart rate response to ACE inhibition is not related to a profound sympatho‐inhibitory effect or an impairment of baroreflex function. While there is some evidence of enhanced cardiac parasympathetic tone it seems unlikely that this is the sole explanation for the lack of cardioacceleration.

show abstract

The effect of captopril on the reflex control heart rate: possible mechanisms.

Cited by 56 publications

References 18 publications

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

The pharmacodynamics and dose‐response relationships of the angiotensin converting enzyme inhibitor, cilazapril, in essential hypertension.

The influence of cilazapril on indices of autonomic function in normotensives and hypertensives.

Contact Info

Product

Resources

About