Atrial natriuretic factor in essential hypertension and adrenal disorders.

Abstract

AKIRA SUGAWARA, KAZUWA NAKAO, TSUYOSHI KONO, NARTTO MORD, TAKAYUKI YAMADA, HIROSHI ITOH, SHOZO SHIONO, YOSHIHIKO SATTO, MASASHI MUKOYAMA, HIROSHI ARAI, AND Hmoo IMURA SUMMARY Patients with untreated essential hypertension had significantly higher plasma atrial natriuretic factor (ANF) levels (92.9 ± 12.9 pg/ml, mean ± SE) than those of age-matched controls (37.8 ± 6.0 pg/ml; p<0.01). Plasma ANF levels in essential hypertensive patients showed a significant positive correlation with mean arterial pressure (MAP; r = 0.46, p<0.05) and an inverse correlation with plasma renin activity (PRA; r = -0.43, p<0.05). Plasma ANF levels after medication showed significant correlation with the decrease hi MAP (r = 0.565, p<0.05). Patients with primary aldosteronism had significantly higher plasma ANF levels (122.4 ± 30.2 pg/ml, a = 8) than those of controls (p<0.05). The levels returned to normal after extirpation of adrenal tumors. The response of plasma ANF levels in patients with primary aldosteronism to volume expansion with infusion of 2 L of physiological saline in 2 hours was greater than hi controls. Such exaggerated response disappeared after surgical treatment. Infusion of angiotensin II (Ang II; 20 ng/kg/min) or norepinephrine (200 ng/kg/min) for 30 minutes to normal volunteers (n = 5) resulted hi a rise hi MAP (24.9 ± 3.3 and 15.8 ± 4.4 mm Hg, respectively) and a twofold increase in plasma ANF level. Infusion of the Ang II antagonist [Sar l ,De r |Ang II (600 ng/kg/min) for 30 minutes, resulted hi a rise hi MAP (18.8 ± 2 . 1 mm Hg) and more than a twofold increase ui plasma ANF level in patients with essential hypertension (n = 6). The increase in the plasma ANF level by the agonistic pressor action of the Ang II antagonist significantly correlated with the increase in MAP (r = 0.760, p<0.05). These results suggest that the plasma ANF level is one of the important clinical parameters for evaluating the hemodynamic state hi essential hypertension, primary aldosteronism, and other adrenal disorders. (Hypertension 11 [Suppl I]: I-212-I-216, 1988)

Proposition of a Feasible Protocol to Evaluate Salt Sensitivity in a Population-Based Setting.

“…ANP during salt loading and ∆ ANP were both significantly correlated with ∆ MBP in the total subjects and subjects 60 years ( p 0.0018-0.005), and ∆ ANP was a significant predictor of ∆ MBP by multiple regression analysis ( p 0.01). In agreement with a previous study (21), there was a significant inverse correlation between PRA and ANP in our study (r 0.35, p 0.002) (Fig. 3).…”

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

“…Decreases of and the degree of pre-existing target organ damage of individual hypertensive patients determines the plasma ANP by atenolol and other beta-blockers, reported in a few patients, 40,42 may be explained if effects of treatment on plasma ANP. The multivariate model in our patients supports this view, and these agents improved severely impaired diastolic relaxation or controlled severe hypertension.…”

“…Moreover, neither PRA before treatment nor the renin status of the patients results could be explained on the basis of differ- ences in the pharmacologic profiles of individual in the rat. 44 Also, infusion of angiotensin II, at pressor 42 or subpressor 45 doses, increases plasma agents within the same family. However, this possibility has also been disproved by reports in which ANP in humans and dogs, respectively.…”

“…It is noteworthy that the latter This is consistent with the majority of studies on the effects of beta-blockers on plasma ANP. [1][2][3] Because relationship predicted a decrease in ANP by zofenopril in patients with pretreatment ANP у45 pg/ml, noradrenaline infusion 42 and shortening of diastole by tachycardia 43 stimulate release of ANP, blockade a value almost identical to mean plasma ANP in our normotensive controls. of adrenergic beta-receptors or reduction of heart rate by atenolol cannot explain our results.…”

Responses of Plasma Catecholamines, Renin-Angiotensin-Aldosterone System, and Atrial Natriuretic Peptide to Exercise in Patients with Essential Hypertension

“…3) fur ther supports the notion that there is a reciprocal relation ship between the RAA system and ANP. Indeed, inverse relationships between PRA and ANP were previously reported in essential HT at rest [38,43], Ganau et al [38] and Sugawara et al [43] reported that plasma ANP levels were inversely related to PRA with coefficients of correla tion o f -0.40 and -0.43, respectively. Our findings of a weak inverse correlation between PRA and ANP (r value o f -0.41) were consistent with their findings.…”