Cardiovascular Pressor Reactivity After Chronic Converting Enzyme Inhibition

Abstract

In addition to inhibiting the formation of angioten sin II, chronic converting enzyme inhibition may affect other blood pressure modulating factors. The influence of an 8 week treatment phase with Cilaza pril on the activity of the renin-angiotensin-aldos terone and sympathetic nervous systems, the pres sor reactivity to infused angiotensin II or norepinephrine, the chronotropic response to iso proterenol, and body sodium and plasma atrial na triuretic peptide concentrations was assessed in 11 normal subjects and 12 patients with essential hy pertension. As compared to a 4 week placebo phase, Cilazapril decreased arterial pressure in both study groups (from 124/83 ± 9/6 to 114/77 ± 9/5 mm Hg and from 143/102 ± 13/7 to 137/96 ± 10/10 mm Hg; Ρ < .025); exchangeable sodium (-158 mmol and, respectively,-104 mmol) and upright plasma al dosterone (-24% and-15%) also tended to fall. Heart rate, the chronotropic response to posture or isoproterenol, plasma norepinephrine levels, the concentration/pressor response curve to norepi nephrine, plasma atrial natriuretic peptide concen tration, plasma angiotensin II and the responses of blood pressure or plasma aldosterone to angiotensin II were unchanged after 8 weeks of Cilazapril. Plasma renin activity increased (+175% to + 650%). These findings indicate that the blood pressure lowering effect of Cilazapril in the stable phase of pharmacological intervention is not associated with modifications of sympathetic-dependent pressor re activity or ^-adrenergic sensitivity. Plasma angio tensin II concentration and angiotensin II-dependent pathways including the pressor and aldosterone responsiveness to angiotensin II are also unchanged.

The effects of atenolol and zofenopril on plasma atrial natriuretic peptide are due to their interactions with target organ damage of essential hypertensive patients

“…For example, hydrochlorothiazide and the major determinants of the effect of ACE inhibitors, the latter should consistently reduce circulating dihydropyridine calcium channel blocker nifedipine have been shown to increase or decrease circullevels of ANP. Neither previous studies, 11,13,15,19 nor our data with zofenopril support this contention. ating ANP.…”

“…3,4 However, the ANP response to beta-blockin patients 10,11 or rats 12,13 with left ventricular dysade is far from consistent. There are many reports function, humans 14,15 or rats 16,17 with hypertension, of unaltered plasma levels of ANP after use of betaand normal subjects. 18,19 A few authors have blockers in patients with heart disease, 5 hypertendescribed increased plasma ANP or ANP/ sion, 6 renal replacement therapy 7 and cardiac transpulmonary capillary wedge pressure ratios after plantation.…”