The effect of enalapril on baroreceptor mediated reflex function in normotensive subjects.

Jf, Giudicelli; Berdeaux, Alain; Édouard, A.; Richer, Christine; Jacolot, D.

doi:10.1111/j.1365-2125.1985.tb05063.x

Cited by 59 publications

(24 citation statements)

References 26 publications

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“…The same finding was reported in normotensive man by Giudicelli et al (1985) and they also concluded that resetting of the baroreflexes accounted for the lack of reflex tachycardia during enarapril treatment. However, such baroreflex resetting would not fully explain the finding that norepinephrine abolished the production of reflex tachycardia by captopril in rabbits.…”

Section: Discussionsupporting

confidence: 80%

Role of Norepinephrine in the Lack of Reflex Tachycardia after Angiotensin Converting Enzyme Inhibitor Treatment.

Yagi

Ichikawa²,

Sakamaki

et al. 1992

Tohoku J. Exp. Med.

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Angiotensin converting enzyme inhibitors decrease blood pressure without causing reflex tachycardia in hypertensives, but do not always do so in normotensives. To investigate this phenomenon, hemodynamic changes in normotensive rabbits receiving a subpressor dose of norepinephrine were studied following captopril or diltiazem treatment. We also investigated the effect of captopril on baroreceptor reflex in relation to norepinephrine infusion ; the baroreflex sensitivity was determined by the relationship between mean arterial pressure and pulse interval receiving graded doses of phenylephrine. Captopril infusion decreased mean arterial pressure and pulse interval from 84+4 to 74+5 mmHg and 244± 7.4 to 216± 7.6 msec, respectively. In contrast, in rabbits receiving a norepinephrine infusion captopril lowered mean arterial pressure to the same extent (92 + 5 to 76 + 3 mmHg, p <0.05) without producing reflex tachycardia. When diltiazem was administered, reflex tachycardia occurred in rabbits both with and without a norepinephrine infusion. There was no difference in the baroreflex sensitivity between rabbits receiving norepinephrine with and without captopril treatment. However, the baroreflex curve showed a slight shift to lower pressures after norepinephrine infusion in the rabbits receiving captopril. These results suggest that elevating circulating norepinephrine might be involved in preventing reflex tachycardia after captopril.captopril ; heart rate ; norepinephrine ; bradykinin It has been well documented that angiotensin converting enzyme inhibitors decrease blood pressure in hypertensive patients and animals without accompanying reflex tachycardia (Duhme 1974;Bengis et al. 1978 ;Fagard et al. 1980 ;

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Section: Discussionsupporting

confidence: 80%

Role of Norepinephrine in the Lack of Reflex Tachycardia after Angiotensin Converting Enzyme Inhibitor Treatment.

Yagi

Ichikawa²,

Sakamaki

et al. 1992

Tohoku J. Exp. Med.

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“…16 One of the characteristics of ACEis is that they lower peripheral vascular resistance without causing a compensatory increase in heart rate [17][18][19][20] or changing baroreceptor activity. 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.…”

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 99%

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

2009

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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.

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“…In a recent article in the Journal, Giudicelli et al (1985) reported on the influence of enalapril on baroreflexes in an attempt to explain the absence of tachycardia with blood pressure reduction, a characteristic haemodynamic feature of angiotensin converting enzyme (ACE) inhibitors. Their focus was mainly on baroreceptor reflexes, hence their article somehow obscures other possible explanations for the absence of reflex cardioacceleration including (1) a central sympatho-inhibitory action, (2) removal of the peripheral angiotensin II (All) mediated presynaptic facilitation of noradrenaline release, (3) unchanged arterial wall tangential tension during ACE inhibition, (4) selective venodilatation or (5) parasympathetic activation.…”

mentioning

confidence: 99%