The relationship of the renal vascular activity of angiotensin II to the autonomic nervous system.

McGiff, John C.; Fasy, T M

doi:10.1172/jci105297

Cited by 45 publications

(21 citation statements)

References 21 publications

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“…Normal subjects respond to angiotensin with a decrease in sodium excretion, in contrast to subjects with hypertension (4,6,14,48) and cirrhosis with ascites (22) who respond with an increase. This same dual action of angiotensin has been demonstrated in animals in which the conditions of salt loading (2,17,19,32) osmotic diuresis (2,8,19), pentobarbital anesthesia (8,23), sympathetic blockade (28), and high doses of drug (2,8,18,21) have been associated with a natriuretic response. The antinatriuretic action of angiotensin has been related to both a fall in glomerular filtration rate (GFR) (6,31,34,36) and an increase in production o f aldosterone (1,4,9,44).…”

Section: Introductionsupporting

confidence: 61%

Action of Angiotensin in Normal, Adrenalectomized, and Renal Hypertensive Trained Dogs

He¹

1968

Nephron

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The relationship between filtration rate (GFR) and electrolyte excretion was investigated during infusions of low doses of angiotensin II (0.02 to 2.0 µg/sq m/min) by means of repeated clearance experiments in trained normal, adrenalectomized, and chronic experimental renal hypertensive dogs. A limited number of experiments were conducted also in dogs anesthetized with pentobarbital. Parameters of BP, C_In, C_pAH, U_Na, and U_k were determined simultaneously under conditions of a moderate water diuresis. Alterations in GFR were produced by varying the dose of angiotensin, thereby allowing a study of electrolyte excretion under conditions of decreased, relatively unchanged, and increased filtered loads. The data was grouped for statistical analysis on the basis of whether the change in GFR from control was more than –5%, within ± 5%, or above +5%. Sodium excretion (U_NaV) was found to parallel the change in GFR in the three types of dogs. Potassium excretion (U_kV) showed also a relationship with GFR in the normal and hypertensive dogs but fell significantly below control in the adrenalectomized dogs when GFR remained at control levels (within ± 5%). Significant alterations in tubular sodium transport were not apparent at the low doses of angiotensin used in this study. A dampened renal vasomotor response was observed in the hypertensive dogs which was associated with a greater tendency of GFR to increase above control. It is concluded that under the conditions of this study low doses of angiotensin can produce a decrease, no change, or an increase in the excretion of sodium as a result of the drug’s action on the renal vascular bed to alter GFR.

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Section: Introductionsupporting

confidence: 61%

Action of Angiotensin in Normal, Adrenalectomized, and Renal Hypertensive Trained Dogs

He¹

1968

Nephron

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“…The fact that the increase in uterine blood flow with angiotensin was blocked by propranolol indicates that angiotensin stimulates beta adrenergic fibers in the uterus. The effect of angiotensin in certain vascular beds is known to be dependent upon the autonomic nervous system (24)(25)(26). In the hand and foot, vasoconstriction with angiotensin is due mainly to its sympathetic effect and is suppressed by alpha adrenergic blocking drugs.…”

Section: Methodsmentioning

confidence: 99%

Uterine blood flow and uterine renin secretion

Ferris¹,

Stein²,

Kauffman³

1972

J. Clin. Invest.

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“…[1][2][3][4][5][6][7][8][9] The intracerebroventricular (ICV) administration of Ang II causes a dose-related increase in blood pressure (BP), 10 which is probably related to activation of Ang II type 1 (AT 1 ) receptors localized in the median preoptic nucleus and juxtaventricular neurons of the subfornical organ and organum vasculosum laminae terminalis 11,12 and the brain stem. 13 Ang II of central origin may activate peripheral sympathetic nerve activity trough a decrease of the arterial baroreceptor gain 14 or activation of preganglionic neurons in the rostral ventrolateral medulla (RVLM) or intermediolateral column.…”

mentioning

confidence: 99%

Downregulation of Neuronal Nitric Oxide Synthase and Interleukin-1β Mediates Angiotensin II-Dependent Stimulation of Sympathetic Nerve Activity

Campese

Zhong

2002

Hypertension

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Abstract-There is substantial evidence that angiotensin II (Ang II) enhances sympathetic nervous system (SNS) activity.We recently observed that nitric oxide and interleukin-1␤ (IL-1␤) exert a tonic inhibitory action on central SNS activity. Moreover, in 2 rat models of neurogenic hypertension, one caused by intrarenal injection of phenol and the other by 5/6 nephrectomy, we observed that losartan, an Ang II type 1 receptor blocker, inhibits SNS activity and increases the abundance of IL-1␤ and the neuronal isoform of nitric oxide synthase (nNOS) in the posterior hypothalamic nuclei (PH), paraventricular nuclei (PVN), and locus ceruleus (LC). This raises the possibility that the stimulatory effects of Ang II on central SNS activity may be mediated by inhibition of nNOS and IL-1␤. To test this hypothesis, we studied the effect of an intracerebroventricular (ICV) infusion of Ang II on blood pressure (BP), norepinephrine (NE) secretion from the PH, renal SNS activity (RSNA), and abundance of IL-1␤ and nNOS mRNA in the PH, PVN, and LC of normal Sprague-Dawley rats. Finally, we measured the concentration of nitrite/nitrate in the dialysate collected from the PH after Ang II or vehicle. ICV infusion of Ang II (100 ng/kg body wt dissolved in 10 L of artificial cerebrospinal fluid) raised BP, RSNA, and NE secretion from the PH compared with control rats. Ang II reduced the abundance of IL-1␤ and nNOS mRNA in the PH, PVN, and LC. Pretreatment with losartan (10 g/kg body wt dissolved in 10 L of aCSF) given ICV 20 minutes before Ang II abolished the effects of Ang II on BP, RSNA, and NE secretion from the PH and IL-1␤ and nNOS mRNA. Ang II also decreased the secretion of NO from the PH. In conclusion, these studies suggest that Ang II inhibits the expression of IL-1␤ and nNOS in the brain. Because locally produced NO exerts a tonic inhibitory action on SNS activity, the decrease in NO expression caused by Ang II results in greater SNS activity. Key Words: angiotensin II Ⅲ sympathetic nervous system Ⅲ losartan Ⅲ nitric oxide Ⅲ interleukins T here is substantial evidence that angiotensin II (Ang II) enhances sympathetic nervous system (SNS) activity via actions on the brain, sympathetic ganglia, and sympathetic nerve endings. 1-9 The intracerebroventricular (ICV) administration of Ang II causes a dose-related increase in blood pressure (BP), 10 which is probably related to activation of Ang II type 1 (AT 1 ) receptors localized in the median preoptic nucleus and juxtaventricular neurons of the subfornical organ and organum vasculosum laminae terminalis 11,12 and the brain stem. 13 Ang II of central origin may activate peripheral sympathetic nerve activity trough a decrease of the arterial baroreceptor gain 14 or activation of preganglionic neurons in the rostral ventrolateral medulla (RVLM) or intermediolateral column. 15 Agents that inhibit the renin-angiotensin system (angiotensin-converting enzyme inhibitors and Ang II AT 1 -receptor antagonists) may provide important information on the effects and site of action of Ang I...

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The relationship of the renal vascular activity of angiotensin II to the autonomic nervous system.

Cited by 45 publications

References 21 publications

Action of Angiotensin in Normal, Adrenalectomized, and Renal Hypertensive Trained Dogs

Action of Angiotensin in Normal, Adrenalectomized, and Renal Hypertensive Trained Dogs

Uterine blood flow and uterine renin secretion

Downregulation of Neuronal Nitric Oxide Synthase and Interleukin-1β Mediates Angiotensin II-Dependent Stimulation of Sympathetic Nerve Activity

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