Increased pressor function of central vasopressinergic system in hypertensive renin transgenic rats

Szczepañska‐Sadowska, Ewa; Paczwa, Piotr; Lon, S.; Ganten, Detlev

doi:10.1097/00004872-199816100-00016

Cited by 27 publications

(22 citation statements)

References 18 publications

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“…In other words, angiotensin II activation is necessary for V1 receptors to elicit a pressor effect in BHR. These results obtained by peripheral application of an angiotensinconverting enzyme inhibitor are at least partially similar to those in a report showing that centrally released vasopressin is involved in mediation of the pressor effect exerted by centrally applied angiotensin II in renin transgenic hypertensive rats (11). On the other hand, the depressor effects of an angiotensin-converting enzyme inhibitor, derapril, are greater in the case of central administration than in the case of oral administration, although in the case of either central or oral administration there is no difference in the changes in systolic blood pressure between derapril-and V1A treated SHR (28).…”

Section: Discussionsupporting

confidence: 89%

“…In addition, it has recently been demonstrated that centrally released arginine vasopressin (AVP) is involved in mediation of the pressor effect exerted by centrally applied angiotensin II in renin transgenic hypertensive rats (11). This report suggested that the renin-angiotensin system may be a key factor in V1 receptor activation in hypertensive animals.…”

Section: Introductionmentioning

confidence: 99%

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Contribution of Endogenous Vasopressin to Regional Hemodynamics in Borderline-Hypertensive Hiroshima Rats

et al. 2002

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by a high plasma concentration of vasopressin, exogenous vasopressin-induced hyperpressor action and cardiac hypertrophy. We proposed that hypertension in BHR is caused by an abnormality in vasopressin-mediated vasoconstriction.There are several lines of evidence showing that vasopressin plays an important role in the development and maintenance of hypertension in spontaneously hypertensive rats (SHR) (2-7). Naitoh et al. (8) reported the involvement of vasopressin V1 receptor-mediated pressor action in the pathogenesis of hypertension in SHR. On the other hand,

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Contribution of Endogenous Vasopressin to Regional Hemodynamics in Borderline-Hypertensive Hiroshima Rats

et al. 2002

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“…There is a general consensus that central administration of these peptides heightens the sympathetic drive and exerts significant pressor effects (DiBona 1999;Ganten et al 1985;Janiak et al 1989;Łoń et al 1996;Noszczyk et al 1993;Paczwa et al 1997). In addition, increasing evidence indicates that ANG II may be involved in resetting central cardiovascular control in various models of hypertension, and in post-infarct cardiac failure (Cudnoch-Jedrzejewska et al 2007; Kagiyama et al 2001;Kubo et al 2000;Leenen et al 1999;Szczepanska-Sadowska et al 1998; Wang and Ma 2000;Zhang et al 1999;Zhu et al 2004;Zucker et al 2004). With regard to post-infarct cardiac failure, it has been established that a blockade of central AT1 receptors for ANG II and V1a receptors for VP significantly reduces MABP and renal sympathetic nerve activity in rats with a myocardial infarct while the same procedure was not effective in shamoperated rats (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Leenen et al 1999;Zhang et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Differential sensitisation to central cardiovascular effects of angiotensin II in rats with a myocardial infarct: Relevance to stress and interaction with vasopressin

Cudnoch‐Jędrzejewska

Szczepañska‐Sadowska

Dobruch

et al. 2008

Stress

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The purpose of the present study was to elucidate if rats with myocardial infarction manifest altered responsiveness to central cardiovascular effects of low doses of angiotensin II (ANG II), and if ANG II and vasopressin (VP) cooperate in the central regulation of cardiovascular functions at rest and during stress. Conscious Sprague-Dawley rats with myocardial infarction induced by left coronary artery ligation, or sham-ligated (SL) controls were infused intracerebroventricularly with artificial cerebrospinal fluid (aCSF), ANG II, ANG II + VP or ANG II + V1a receptor antagonist (V1ANT) 4 weeks after cardiac surgery. In the infarcted but not in the SL rats, the resting mean arterial blood pressure (MABP) was significantly elevated by infusions of ANG II and ANG II + VP, while infusion of ANG II + V1ANT was not effective. During administration of aCSF, the pressor, and tachycardic responses to an air-jet stressor were significantly greater in the infarcted than in the SL rats. In the SL rats, the pressor responses to the stressor were significantly greater during infusions of ANG II, ANG II + VP and ANG II + V1ANT than during infusion of aCSF. The tachycardic response in the SL rats was enhanced only by the combined infusion of ANG II + VP. In the infarcted rats, the pressor and the tachycardic responses to the stressor were similar in all groups. It is concluded that: (1) under resting conditions the infarcted rats manifest sensitisation to the central pressor effect of ANG II and that this effect depends on concomitant stimulation of V1a VP receptors, (2) central ANG II may enhance the pressor response to an alarming stressor in the SL rats through an action which does not depend on the concomitant stimulation of V1a receptors, (3) the cooperative action of ANG II and VP is required for intensification of the tachycardic response to the alarming stressor in the SL rats and (4) exaggeration of the cardiovascular responses to the alarming stressor in the infarcted rats cannot be further augmented by an additional stimulation of central ANG II receptors or combined stimulation of ANG II and VP receptors.

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“…suppressed (29,38,50) plasma renin models, psychogenic (42), cold exposure (61), renal injury (73), sleep apnea (12) models, transgenic TGR (mRen2)27 rats (62), and both Dahl salt-sensitive (29) and spontaneously hypertensive rats (SHR) maintained on high-salt diets (37,47,72). Two major mechanisms have been documented that account for the blood pressure effects of brain angiotensin.…”

mentioning

confidence: 99%

“…Two major mechanisms have been documented that account for the blood pressure effects of brain angiotensin. First, actions of the RAS within the supraoptic (SON) and paraventricular hypothalamic nuclei (PVN) stimulate the production and release of arginine vasopressin (AVP, also known as antidiuretic hormone, ADH, or argipressin) (4,10,17,31,51,53,62). Second, hindbrain and brain stem actions of the RAS alter baroreflex function and sympathetic output (22,26).…”

mentioning

confidence: 99%

Hypertension in mice with transgenic activation of the brain renin-angiotensin system is vasopressin dependent

Littlejohn¹,

Siel²,

Ketsawatsomkron³

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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An indispensable role for the brain renin-angiotensin system (RAS) has been documented in most experimental animal models of hypertension. To identify the specific efferent pathway activated by the brain RAS that mediates hypertension, we examined the hypothesis that elevated arginine vasopressin (AVP) release is necessary for hypertension in a double-transgenic model of brain-specific RAS hyperactivity (the "sRA" mouse model). sRA mice experience elevated brain RAS activity due to human angiotensinogen expression plus neuron-specific human renin expression. Total daily loss of the 4-kDa AVP prosegment (copeptin) into urine was grossly elevated (≥8-fold). Immunohistochemical staining for AVP was increased in the supraoptic nucleus of sRA mice (~2-fold), but no quantitative difference in the paraventricular nucleus was observed. Chronic subcutaneous infusion of a nonselective AVP receptor antagonist conivaptan (YM-087, Vaprisol, 22 ng/h) or the V(2)-selective antagonist tolvaptan (OPC-41061, 22 ng/h) resulted in normalization of the baseline (~15 mmHg) hypertension in sRA mice. Abdominal aortas and second-order mesenteric arteries displayed AVP-specific desensitization, with minor or no changes in responses to phenylephrine and endothelin-1. Mesenteric arteries exhibited substantial reductions in V(1A) receptor mRNA, but no significant changes in V(2) receptor expression in kidney were observed. Chronic tolvaptan infusion also normalized the (5 mmol/l) hyponatremia of sRA mice. Together, these data support a major role for vasopressin in the hypertension of mice with brain-specific hyperactivity of the RAS and suggest a primary role of V(2) receptors.

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Increased pressor function of central vasopressinergic system in hypertensive renin transgenic rats

Cited by 27 publications

References 18 publications

Contribution of Endogenous Vasopressin to Regional Hemodynamics in Borderline-Hypertensive Hiroshima Rats

Contribution of Endogenous Vasopressin to Regional Hemodynamics in Borderline-Hypertensive Hiroshima Rats

Differential sensitisation to central cardiovascular effects of angiotensin II in rats with a myocardial infarct: Relevance to stress and interaction with vasopressin

Hypertension in mice with transgenic activation of the brain renin-angiotensin system is vasopressin dependent

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