The effect of chronic captopril therapy on adrenergic receptors, plasma noradrenaline and the vascular responses to infused noradrenaline

Kondowe, G B; Copeland, Shannon; Passmore, Anthony Peter; Leahey, William J.; Johnston, G D

doi:10.1007/bf00607568

Cited by 7 publications

(4 citation statements)

References 22 publications

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Section: Resultsmentioning

confidence: 48%

“…Kondowe et al, 1987). From the human data presented by Kondowe et al, 1987, and substantiated by our study, we were not able to detect changes in the response to noradrenaline at trough concentrations of the ACE inhibitor. However, at cilazaprilat peak concentrations, a small shift to the right of the noradrenaline response curve was detected in our volunteers, exerting a DR-1 of 0.69 (95% confidence intervals 0.13-2.18).…”

Section: Resultsmentioning

confidence: 48%

“…However, their combination is generally not recommended for treating hypertension (Zanchetti, 1987) since both drugs presumably act at least in part via the same mechanism, namely, by suppressing the renin-angiotensin-system and by interfering with the sympathetic system (Douglas, 1985;MacGregor et al, 1985;Kondowe et al, 1987). However, in the treatment of various diseases, a combined use of the two drug groups is sometimes unavoidable.…”

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confidence: 99%

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Interactions between cilazapril and propranolol in man; plasma drug concentrations, hormone and enzyme responses, haemodynamics, agonist dose‐effect curves and baroreceptor reflex.

Belz¹,

Essig²,

Kleinbloesem³

et al. 1988

Brit J Clinical Pharma

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1. The pharmacokinetics, hormonal and haemodynamic responses at rest and during challenges with angiotensin I (blood pressure), isoprenaline (heart rate), and noradrenaline (blood pressure) were investigated in six healthy male volunteers following a 1 week treatment with placebo, propranolol (120 mg day‐1), cilazapril (2, 5 mg day‐1), and a combination of both in a double‐blind cross‐over design. 2. Both drugs reduced systolic and diastolic blood pressure by about 7 mm Hg as compared with placebo. After coadministration, this drop in blood pressure was doubled and lasted longer than after the administration of the individual components. 3. Following cilazapril, a pronounced increase in plasma renin activity (PRA) was found (factor approximately 10 at drug peak concentrations). Coadministration of both drugs resulted only in a moderate increase in the PRA (factor approximately 3). Significant changes in plasma catecholamines were not observed. 4. Propranolol shifted the isoprenaline dose‐effect curve to the right, and cilazapril that of angiotensin I, irrespective of the presence of the other drug. Cilazapril tended to shift the noradrenaline dose‐ effect curve somewhat to the right. 5. The gain of the baroreceptor reflex (angiotensin‐stimulation) was not influenced by cilazapril but was lowered by propranolol, irrespective of the presence of the ACE inhibitor. 6. Except for a statistically not significant decrease in the peak concentrations of each drug during the combined therapy, a pharmacokinetic interaction between the two drugs was not found.

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Section: Resultsmentioning

confidence: 48%

Section: Resultsmentioning

confidence: 48%

mentioning

confidence: 99%

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Interactions between cilazapril and propranolol in man; plasma drug concentrations, hormone and enzyme responses, haemodynamics, agonist dose‐effect curves and baroreceptor reflex.

Belz¹,

Essig²,

Kleinbloesem³

et al. 1988

Brit J Clinical Pharma

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“…36 A recent study, however, suggests that the known interaction between the renin-angiotensin and the sympathetic nervous system observed in animals is probably of little significance in humans. 37 The present study demonstrated that sympathetic activation attenuates the effect of captopril on the upper limit of CBF autoregulation. This result could be explained by two different mechanisms: 1) The previously shown effect of captopril on the upper limit of CBF autoregulation could be interpreted as a consequence of impaired constriction by angiotensin II, an effect independent of the sympathetic nervous system.…”

Section: Ace Inhibition and Cbfsupporting

confidence: 58%

Angiotensin converting enzyme inhibition and the upper limit of cerebral blood flow autoregulation: effect of sympathetic stimulation.

Waldemar

Paulson

Barry

et al. 1989

Circulation Research

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The effect of stimulation of the cervical sympathetic ganglia on the upper limit of cerebral blood flow (CBF) autoregulation was studied in normotensive Wistar-Kyoto rats (WKY) and in spontaneously hypertensive rats (SHR) following intravenous administration of the angiotensin converting enzyme inhibitor captopril (10 mg/kg). CBF was measured using the intracarotid 133Xe injection method in halothane/nitrous oxide anaesthetized WKY and SHR. Arterial blood pressure was raised stepwise by the intravenous infusion of noradrenaline. Toward the end of the study, Evans blue was injected and the brains examined for gross blood-brain barrier breakdown. In SHR, sympathetic stimulation reextended the upper limit of CBF autoregulation, which was at a mean arterial blood pressure level of 120-139 mm Hg in the control group of eight SHR and above 170 mm Hg in the stimulated group of nine SHR. In the group of nine WKY subjected to sympathetic stimulation, the upper limit of CBF autoregulation was reached at a mean arterial blood pressure level of 110-129 mm Hg as opposed to 90-109 mm Hg in a previous unstimulated group of WKY. In the two groups subjected to sympathetic stimulation, there was no extravasation of Evans blue in any of the brains. In the control group of SHR, in which there had been marked increases in CBF, three out of eight brains had foci with extravasation of the dye. It is concluded that in normotensive and in hypertensive rats sympathetic stimulation attenuates the downward shift of the upper limit of CBF autoregulation, which is known to accompany intravenous administration of captopril.

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ACE Inhibition and Pressor Responsiveness to Norepinephrine in Hypertensive Patients

Malini

Strocchi

Valtancoli

et al. 1990

The Journal of Clinical Pharma

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The pressor response to norepinephrine (NE) was assessed in normal renin essential hypertensive patients before and after they were randomly assigned to receive in parallel groups of treatment a single dose of an angiotensin converting enzyme (ACE) inhibitor (captopril or lisinopril) or a prolonged therapy with lisinopril (30-45 days) or with hydrochlorothiazide (9 days). Blood pressure was significantly reduced by all treatments. The pressor response to NE was unchanged after the single administration of the ACE inhibitors, while it was blunted after chronic administration of lisinopril and after the diuretic. On the basis of these results, it is suggested that the attenuation of the sympathetically mediated vasoconstriction may represent an additional mechanism contributing to the antihypertensive effect of ACE inhibitors administered chronically.

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The effect of chronic captopril therapy on adrenergic receptors, plasma noradrenaline and the vascular responses to infused noradrenaline

Cited by 7 publications

References 22 publications

Interactions between cilazapril and propranolol in man; plasma drug concentrations, hormone and enzyme responses, haemodynamics, agonist dose‐effect curves and baroreceptor reflex.

Interactions between cilazapril and propranolol in man; plasma drug concentrations, hormone and enzyme responses, haemodynamics, agonist dose‐effect curves and baroreceptor reflex.

Angiotensin converting enzyme inhibition and the upper limit of cerebral blood flow autoregulation: effect of sympathetic stimulation.

ACE Inhibition and Pressor Responsiveness to Norepinephrine in Hypertensive Patients

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