Central hypertensive actions of angiotensin I, II and III in conscious rats.

Kondo, Kazuoki; Okuno, Takashi; Eguchi, Toyohisa; Nakamura, Ryuichi; Saruta, Takao

doi:10.1507/endocrj1954.26.713

Cited by 8 publications

(4 citation statements)

References 11 publications

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“…An alternative interpretation of our findings is that the attenuated pressor response to Ang-[1–8] in the FR group is due to a ceiling effect on the ability of the vessel to vasoconstrict; however, this possibility would be AT 1 R specific since the vasoconstrictor, L-phenylephrine, increased MAP to a similar extent in the FR and CT animals. The normal BP response to Ang-[1–8] infusion is four-fold higher than to an equivalent dose of Ang-[1–10] 35 , 36 , which is similar to our findings in the control animals. In contrast, we found no differences in the pressor response in the FR animals between Ang-[1–10] and Ang-[1–8].…”

Section: Discussionsupporting

confidence: 90%

Role of the Renin Angiotensin System in Blood Pressure Allostasis-induced by Severe Food Restriction in Female Fischer rats

Souza

West

Abreu

et al. 2018

Sci Rep

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Severe food restriction (FR) is associated with blood pressure (BP) and cardiovascular dysfunction. The renin-angiotensin system (RAS) regulates BP and its dysregulation contributes to impaired cardiovascular function. Female Fischer rats were maintained on a control (CT) or severe FR (40% of CT) diet for 14 days. In response to severe FR, BP allostasis was achieved by up-regulating circulating Ang-[1–8] by 1.3-fold through increased angiotensin converting enzyme (ACE) activity and by increasing the expression of AT1Rs 1.7-fold in mesenteric vessels. Activation of the RAS countered the depressor effect of the severe plasma volume reduction (≥30%). The RAS, however, still underperformed as evidenced by reduced pressor responses to Ang-[1–8] even though AT1Rs were still responsive to the depressor effects of an AT1R antagonist. The aldosterone (ALDO) response was also inadequate as no changes in plasma ALDO were observed after the large fall in plasma volume. These findings have implications for individuals who have experienced a period(s) of severe FR (e.g., anorexia nervosa, dieters, natural disasters) and suggests increased activity of the RAS in order to achieve allostasis contributes to the cardiovascular dysfunction associated with inadequate food intake.

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Section: Discussionsupporting

confidence: 90%

Role of the Renin Angiotensin System in Blood Pressure Allostasis-induced by Severe Food Restriction in Female Fischer rats

Souza

West

Abreu

et al. 2018

Sci Rep

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“…Intracranially administered renin or angiotensin II causes water drinking and an increase in blood pressure, and these effects are inhibited by an antagonist of angiotensin II (Epstein et al, 1974 ;Reid and Ramsay, 1975;Kondo et al, 1979). In the present study intraventricular administration of tonin also- KONDO et al Endocrinol.…”

Section: Discussionsupporting

confidence: 49%

“…Even though the central role of angiotensin I is still controversial (Swanson et al, 1973), previous studies have reported that water drinking and increase in blood pressure induced by centrally administered renin or angiotensin I were inhibited by a converting enzyme inhibitor (Severs et al, 1973;Epstein et al, 1974 ;Kondo et al, 1979). The effects of tonin, however, were not inhibited by the simultaneous intraventricular administration of a converting enzyme inhibitor.…”

Section: Discussionmentioning

confidence: 99%

The effects of intracerebroventricular administration of tonin on water drinking and blood pressure in rats.

et al. 1980

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Intraventricularadministration of tonin, an enzyme which forms angiotensin II directly from a natural protein substrate (angiotensinogen), stimulated water drinking and increased systemic blood pressure in rats. These responses were abolished by the simultaneous administration of an angiotensin II analogue, but unaffected by an angiotensin I-converting enzyme inhibitor. We confirmed, in vitro, that angiotensin II was generated when the brain homogenate was incubated with tonin in the presence of DFP and EDTA. These results indicate that the central effects of tonin on water drinking and systemic blood pressure are mediated via the direct formation of angiotensin II in the brain, and suggest the possibility that the tonin-angiotensin II system in the central nervous system might be important in controlling water balance and blood pressure.

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“…The pattern and time course of this hemodynamic response is similar to that produced by AII administered intraventricularly at this dose in other species. 3,34,35 ICV AII caused significant increases in MAP (panels A and B) and reductions in HR (panels C and D) compared with baseline in both groups. The absolute changes in MAP and HR after AII administration were marginally greater (Pϭ0.048 and Pϭ0.046 for MAP and HR, respectively) in RAϩ mice compared with controls.…”

Section: Effects Of Icv Losartan and Aii On Map And Hrmentioning

confidence: 95%

The Brain Renin-Angiotensin System Contributes to the Hypertension in Mice Containing Both the Human Renin and Human Angiotensinogen Transgenes

Davisson

Yang

Beltz

et al. 1998

Circulation Research

136

155

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Abstract-We have previously shown that mice transgenic for both the human renin and human angiotensinogen genes (RAϩ) exhibit appropriate tissue-and cell-specific expression of both transgenes, have 4-fold higher plasma angiotensin II (AII) levels, and are chronically hypertensive. However, the relative contribution of circulating and tissue-derived AII in causing hypertension in these animals is not known. We hypothesized that the brain renin-angiotensin system contributes to the elevated blood pressure in this model. To address this hypothesis, mean arterial pressure (MAP) and heart rate were measured in conscious, unrestrained mice after they were instrumented with intracerebroventricular cannulae and carotid arterial and jugular vein catheters. Intracerebroventricular administration of the selective AII type 1 (AT-1) receptor antagonist losartan (10 g, 1 L) caused a significantly greater peak fall in MAP in RAϩ mice than in nontransgenic RAϪ controls (Ϫ29Ϯ4 versus Ϫ4Ϯ2 mm Hg, PϽ0.01). To explore the mechanism of a central renin-angiotensin system-dependent hypertension in RAϩ mice, we determined the relative depressor responses to intravenous administration of the ganglionic blocking agent hexamethonium (5 mg/kg) or an arginine vasopressin (AVP) V 1 receptor antagonist (AVPX, 10 g/kg). Hexamethonium caused equal lowering of MAP in RAϩ mice and controls (Ϫ46Ϯ3 versus Ϫ52Ϯ3, PϾ0.05), whereas AVPX caused a significantly greater fall in MAP in RAϩ compared with RAϪ mice (Ϫ24Ϯ2 versus Ϫ6Ϯ1, PϽ0.01). Consistent with this was the observation that circulating AVP was 3-fold higher in RAϩ mice than in control mice. These results suggest that increased activation of central AT-1 receptors, perhaps those located at sites involved in AVP release from the posterior pituitary gland, plays a role in the hypertension in RAϩ mice. Furthermore, our finding that both human transgenes are expressed in brain regions of RAϩ mice known to be involved in cardiovascular regulation raises the possibility that augmented local production of AII and increased activation of AT-1 receptors at these sites is involved. (Circ Res. 1998;83:1047-1058.)Key Words: transgenic mice Ⅲ angiotensin Ⅲ blood pressure Ⅲ genetics Ⅲ pharmacology I t is well established that blood-borne angiotensin II (AII), the effector peptide of the renin-angiotensin system (RAS), plays a major role in the regulation of arterial blood pressure (BP) and volume homeostasis through its interaction with specific AII receptors present in vascular smooth muscle, kidney, and adrenal gland. Stimulation of these peripheral AII receptors leads to elevations in BP through increased vascular resistance, cardiac output, sodium reabsorption, and blood volume.1 However, in addition to these well-known actions at peripheral sites, AII also contributes to BP and volume regulation through its receptor-mediated effects on neurons located within the central nervous system (CNS). Indeed, central administration of AII causes increases in BP, antidiuresis, drinking, and salt appetite.2 This, ...

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Central hypertensive actions of angiotensin I, II and III in conscious rats.

Cited by 8 publications

References 11 publications

Role of the Renin Angiotensin System in Blood Pressure Allostasis-induced by Severe Food Restriction in Female Fischer rats

Role of the Renin Angiotensin System in Blood Pressure Allostasis-induced by Severe Food Restriction in Female Fischer rats

The effects of intracerebroventricular administration of tonin on water drinking and blood pressure in rats.

The Brain Renin-Angiotensin System Contributes to the Hypertension in Mice Containing Both the Human Renin and Human Angiotensinogen Transgenes

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