Central action of atrial natriuretic polypeptide on blood pressure in conscious rats

Itoh, Hiroshi; Nakao, Kazuwa; Morii, Narito; Yamada, Takayuki; Shiono, Satoshi; Sakamoto, Makoto; Sugawara, Akira; Saito, Yoshihiko; Katsuura, Goro; Shiomu, Teruo; Eigyo, Masami; Matsushita, Akira; Imura, Hiroo

doi:10.1016/0361-9230(86)90147-4

Cited by 69 publications

(9 citation statements)

References 22 publications

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“…Thus ANF at the low dose used in the present study was able to antagonize the pressor effect of central Ang II but not its effect on AVP secretion. Similar antagonism by ANF of the pressor effect and the dipsogenic action of central Ang II has been reported in conscious rats (Nakmura et al 1985;Itoh et al 1986). However, those effects were achieved by administration of ANF at doses ranging from 200 ng to 5 Iug, which compares with the infusion rate of 0 4 ng/min in the current work.…”

Section: Discussionsupporting

confidence: 78%

The renal and vascular effects of central angiotensin II and atrial natriuretic factor in the anaesthetized rat.

Al-Barazanji

Balment

1990

The Journal of Physiology

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SUMMARY1. The interaction between atrial natriuretic factor (ANF) and angiotensin II (Ang II) within the brain to influence renal function and blood pressure was studied in Inactin-anaesthetized male Sprague-Dawley rats.2. Central infusion of ANF produced a diuresis which was associated with a significant decrease in plasma arginine vasopressin (AVP) level. There was no change in sodium excretion rate over the 80 min of intracerebroventricular ANF infusion and ANF produced no detectable change in mean arterial blood pressure.3. Central Ang II administration produced a significant decrease in urine flow, which was associated with elevated plasma AVP, an increase in sodium excretion and a rise in mean arterial blood pressure.4. Combined ANF and Ang II infusion produced an antidiuresis, which was associated with increased plasma AVP concentration. Both the natriuretic and vasopressor actions of central Ang II were abolished when ANF was co-administered.5. It is concluded that ANF and Ang II interact centrally; ANF antagonizes the pressor and natriuretic effects but not the antidiuretic effects of central Ang II. These data suggest the possibility of distinct and separate sites within the brain through which Ang II influences vasopressin release and renal sodium handling and elevates blood pressure.

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Section: Discussionsupporting

confidence: 78%

The renal and vascular effects of central angiotensin II and atrial natriuretic factor in the anaesthetized rat.

Al-Barazanji

Balment

1990

The Journal of Physiology

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“…We also demonstrated the wide distribution of ANF in the brain by RIA and immunohistochemistry 8 ' n -n and its prevalence in the anteroventral third ventricular (AV3V) region, and we showed that brain ANF is involved in central cardiovascular control alone or in combination with the brain renin-angiotensin system."" 13 These findings indicate that ANF is a possible endogenous antihypertensive agent.…”

mentioning

confidence: 90%

Atrial natriuretic factor in essential hypertension and adrenal disorders.

et al. 1988

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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)

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“…injection of 100 ng of Ang II (maximal increase of mean arterial pressure: 21.4 ±1.1 mm Hg). 16 The Ang Il-induced pressor response was reported to be due to both the release of AVP and increased sympathetic outflow, 12 based on the previous report that showed that the pressor response to central Ang II was suppressed by the pretreatment of the V,-receptor antagonist of AVP and prazosin. We also observed an increase of plasma catecholamine levels after i.c.v.…”

Section: Discussionmentioning

confidence: 99%

Brain renin-angiotensin. Central control of secretion of atrial natriuretic factor from the heart.

et al. 1988

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HIROSHI ITOH, KAZUWA NAKAO, TAKAYUKI YAMADA, NARITO MORE, SHOZO SHIONO, AKIRA SUGAWARA,. YOSHMKO SAJTO, MASASHI MUKOYAMA, HIROSHI ARAI, AND HIROO IMURASUMMARY To elucidate the modulatory role of the brain renln-angiotensin system in the regulation of the secretion of atrial natriuretic factor (ANF) from the heart, the effects of intracerebroventricular administration of angiotensin II on the plasma ANF level were examined in conscious unrestrained rats. Administration of angiotensin II in doses of 100 ng and 1 fig significantly enhanced ANF secretion induced by volume loading with infusion of 3 ml of saline (peak values of the plasma ANF level: control, 220 ± 57 pg/ml; angiotensin II100 ng, 1110 ± 320 pg/ml, p < 0.01; angiotensin II 1/tg, 1055 ± 60 pg/ml, p<0.01). Injection of angiotensin II alone had no significant effect on the basal plasma ANF level. Central angiotensin H-induced ANF secretion was significantly attenuated by pretreatment with intravenous administration of the V,-receptor antagonist of vasopressin or intracerebroventricular administration of phentolamine. These results indicate that the brain renln-angiotensin system modulates ANF secretion in response to volume loading through the stimulation of vasopressin secretion or the activation of the central a-adrenergic neural pathway. (Hypertension 11 [Suppl I]: I-57-I-61, 1988) KEY WORDS • vasopressin • V, receptor • central nervous system • a-adrenergic system • volume expansion • blood pressure • body fluid homeostasis

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Central action of atrial natriuretic polypeptide on blood pressure in conscious rats

Cited by 69 publications

References 22 publications

The renal and vascular effects of central angiotensin II and atrial natriuretic factor in the anaesthetized rat.

The renal and vascular effects of central angiotensin II and atrial natriuretic factor in the anaesthetized rat.

Atrial natriuretic factor in essential hypertension and adrenal disorders.

Brain renin-angiotensin. Central control of secretion of atrial natriuretic factor from the heart.

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