Activation of central sympathetic neurons by angiotensin II

Keim, Kevin L.; Sigg, E.B.

doi:10.1016/0024-3205(71)90042-7

Cited by 19 publications

(8 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The RAS is generally considered to be activated in obese rodents and humans (for review see 41 ). AngII activates the sympathetic nervous system 42,43 and increases sodium retention, two mechanisms that have been consistently linked to obesity-associated hypertension 2-4 . Given the marked reductions in plasma AngII concentrations in adipocyte AGT deficient mice, it is likely that diminished AngII-mediated regulation of sodium reabsorption and sympathetic nervous system activity contributed to the pronounced effects of adipocyte AGT deficiency to prevent obesity-associated hypertension.…”

Section: Discussionmentioning

confidence: 99%

Adipocyte Deficiency of Angiotensinogen Prevents Obesity-Induced Hypertension in Male Mice

et al. 2012

View full text Add to dashboard Cite

Previous studies demonstrated that diet-induced obesity increased plasma angiotensin II concentrations and elevated systolic blood pressures in male mice. Adipocytes express angiotensinogen and secrete angiotensin peptides. We hypothesize that adipocyte-derived angiotensin II mediates obesity-induced increases in systolic blood pressure in male high fat-fed C57BL/6 mice. Systolic blood pressure was measured by radiotelemetry during week 16 of low fat or high fat feeding in Agtfl/fl and adipocyte-angiotensinogen deficient mice (AgtaP2). Adipocyte angiotensinogen deficiency had no effect on diet-induced obesity. Basal 24 hour systolic blood pressure was not different in low fat-fed Agtfl/fl compared to AgtaP2 mice (124 ± 3 vs. 128 ± 3 mmHg, respectively). In Agtfl/fl mice, high fat feeding significantly increased systolic blood pressure (24 hr; 134 ± 2 mmHg; P<0.05). In contrast, high fat-fed AgtaP2 mice did not exhibit an increase in systolic blood pressure (126 ± 2 mmHg). Plasma angiotensin II concentrations were increased by high fat-feeding in Agtfl/fl mice (low fat, 32 ± 14; high fat, 219 ± 58 pg/ml, P<0.05). In contrast, high fat-fed AgtaP2 mice did not exhibit elevated plasma angiotensin II concentrations (high fat, 18 ± 7 pg/ml). Similarly, adipose tissue concentrations of angiotensin II were significantly decreased in low fat and high fat-fed AgtaP2 mice compared to controls. In conclusion, adipocyte angiotensinogen deficiency prevented high fat-induced elevations in plasma angiotensin II concentrations and systolic blood pressure. These results suggest that adipose tissue serves as a major source of angiotensin II in the development of obesity-hypertension.

show abstract

Section: Discussionmentioning

confidence: 99%

Adipocyte Deficiency of Angiotensinogen Prevents Obesity-Induced Hypertension in Male Mice

et al. 2012

View full text Add to dashboard Cite

show abstract

“…The increment in angiotensin formation should cause sodium retention due to excess aldosterone secretion resulting in further impairment of the lowering of blood pressure by vasodilating drugs alone. Also, angiotensin possesses numerous pharmacologic activities, each of which contribute qualitatively to the elevation of blood pressure (18)(19)(20)(21)(22)(23)(24) and, under certain circumstances, induce pathologic vascular lesions (25,26). Because of these multiple activities of angiotensin, the blockade of renin release by propranolol in 86 PETTINGER, CAMPBELL, KEETON patients treated with vasodilating agents could be an important factor contributing to the efficacy of this drug combination.…”

Section: Discussionmentioning

confidence: 99%

Adrenergic Component of Renin Release Induced by Vasodilating Antihypertensive Drugs in the Rat

Pettinger

Campbell

Keeton

1973

Circulation Research

100

View full text Add to dashboard Cite

The capacity of the vasodilating drugs, minoxidil and hydralazine, for inducing renin release was characterized in rats according to chronology and dose response. Propranolol inhibition of this renin release was also characterized and related to serum levels of propranolol. Minoxidil and hydralazine (1.0 mg/kg) induced sevenfold elevations of serum renin activity. Treatment with propranolol, resulting in plasma propranolol concentrations as low as 50 ng/ml, impaired vasodilatory drug-induced renin release. The propranolol inhibition suggests a beta-adrenergic component to this type of renin release and the potential for a clinically efficacious drug interaction. KEY WORDS hydralazineangiotensin beta-receptor blockade propranolol minoxidil• The combination of a vasodilating drug and propranolol can control hypertension in man without precipitating many untoward effects (1-5).Vasodilating agents elicit renin release from the kidney which results in elevated serum renin activity and increased angiotensin formation (6, 7). The angiotensin thus formed probably antagonizes the antihypertensive effect of vasodilating drugs (8) such as hydralazine and minoxidil. Since combined therapy with propranolol and vasodilating drugs has been found to be particularly effective (1-5), this study was designed to characterize vasodilatory drug-induced renin release in the rat and to determine the effect of beta-receptor blockade on this release.Methods Male Wistar rats (180-250 g) were housed in individual cages and exposed to light by an automated system from 6 AM to 6 PM. The rats ingested tap water and Purina rat chow containing 152 mEq sodium/kg ad libitum.Both hydralazine and minoxidil were administered intraperitoneally, and propranolol was injected subcutaneously. An equal volume (0.5 ml) of saline was administered as a placebo to the control rats. Doses of drugs were calculated for the salt in mg/kg.Propranolol was solubilized in 0.9% NaCl by adding several drops of glacial acetic acid. Propranolol was administered subcutaneously because of the constant, sustained plasma levels following this route of administration (Fig. 1). Intraperitoneal injection of propranolol resulted in a rapid rise and fall and a high degree of variability in serum levels among the rats. Alternatively, subcutaneous administration resulted in more sustained plasma propranolol levels with minimal variability among the rats. Thus, the sustained plateau (Fig. 1) from the subcutaneous administration permitted the experiments to be done at relatively constant, predictable propranolol serum levels.In the experiments involving beta-receptor blockade, propranolol was injected at 0 time and the vasodilating drug was injected at 10 minutes; the rats were decapitated at 30 minutes. The rats treated with a vasodilating drug alone or with saline were killed 20 minutes after injection.At the times indicated in Results, the unanesthetized rats were decapitated, and aortic blood samples were collected in iced, siliconized glass tubes during the first 4 secon...

show abstract

“…The importance of the sympathetic nervous system in mediating central cardiovascular effects of Ang has been recognized since the mid 1960 s in all species studied although relatively few studies have measured nerve activity directly (18). A number of studies suggest that in the rat there is an important contribution to the pressor response by release of vasopressin (19).…”

Section: Cardiovascular Effects Of Intraventricular Angmentioning

confidence: 99%

Angiotensin and baroreflex control of the circulation

Head¹,

Saigusa

Mayorov³

2002

Braz J Med Biol Res

View full text Add to dashboard Cite

There is a close association between the location of angiotensin (Ang) receptors and many important brain nuclei involved in the regulation of the cardiovascular system. The present review encompasses the physiological role of Ang II in the brainstem, particularly in relation to its influence on baroreflex control of the heart and kidney. Activation of AT 1 receptors in the brainstem by fourth ventricle (4V) administration to conscious rabbits or local administration of Ang II into the rostral ventrolateral medulla (RVLM) of anesthetized rabbits acutely increases renal sympathetic nerve activity (RSNA) and RSNA baroreflex responses. Administration of the Ang antagonist Sarile into the RVLM of anesthetized rabbits blocked the effects of Ang II on the RSNA baroreflex, indicating that the RVLM is the major site of sympathoexcitatory action of Ang II given into the cerebrospinal fluid surrounding the brainstem. However, in conscious animals, blockade of endogenous Ang receptors in the brainstem by the 4V AT 1 receptor antagonist losartan resulted in sympathoexcitation, suggesting an overall greater activity of endogenous Ang II within the sympathoinhibitory pathways. However, the RSNA response to airjet stress in conscious rabbits was markedly attenuated. While we found no effect of acute central Ang on heart rate baroreflexes, chronic 4V infusion inhibited the baroreflex and chronic losartan increased baroreflex gain. Thus, brainstem Ang II acutely alters sympathetic responses to specific afferent inputs thus forming part of a potentially important mechanism for the integration of autonomic response patterns. The sympathoexcitatory AT 1 receptors appear to be activated during stress, surgery and anesthesia.

show abstract

Activation of central sympathetic neurons by angiotensin II

Cited by 19 publications

References 9 publications

Adipocyte Deficiency of Angiotensinogen Prevents Obesity-Induced Hypertension in Male Mice

Adipocyte Deficiency of Angiotensinogen Prevents Obesity-Induced Hypertension in Male Mice

Adrenergic Component of Renin Release Induced by Vasodilating Antihypertensive Drugs in the Rat

Angiotensin and baroreflex control of the circulation

Contact Info

Product

Resources

About