Hemodynamic effects of central angiotensin I, II, and III in conscious rabbits

Head, Geoffrey A.; Williams, N. S.

doi:10.1152/ajpregu.1992.263.4.r845

Cited by 27 publications

(30 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The vasoconstriction occurred in both the mesenteric and renal vascular beds but was accompanied by dilatation of the hindlimb vascular bed and a fall in heart rate which opposed the vasoconstriction and reduced the observed pressor response. However, the hindlimb dilatation changed to vasoconstriction in rabbits after sinoaortic denervation, suggesting that it was mainly due to a baroreflex response to the rise in blood pressure (12). …”

Section: Cardiovascular Effects Of Intraventricular Angmentioning

confidence: 95%

“…Bolus injections of Ang II produced dose-dependent increases in blood pressure with doses about 400 times lower than those given intravenously ( Figure 1). The onset of the response was relatively quick, within 1 min, and generally lasted only 5 min, depending on the dose (12). The receptors were AT 1 since the pressor response to Ang II administered into the 4V of conscious rabbits was completely blocked by low doses of the nonpeptide selective antagonist losartan but not affected by the AT 2 antagonist PD123319 (17).…”

Section: Cardiovascular Effects Of Intraventricular Angmentioning

confidence: 99%

“…In this species, however, the site of action involved the anterior ventral third ventricle which correlates well with the location of the receptors and is relatively close to the injection site. In conscious rabbits, however, lateral or third ventricle injections of Ang II had little effect on blood pressure with doses as large as 1000 pmol (Figure 1) (12). The rabbit also does not respond to chronic infusions of Ang into the lateral ventricle (13) nor does acute injection of Ang produce dipsogenic responses (14) as it does in the rat.…”

Section: Cardiovascular Effects Of Intraventricular Angmentioning

confidence: 99%

See 2 more Smart Citations

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

Section: Cardiovascular Effects Of Intraventricular Angmentioning

confidence: 95%

Section: Cardiovascular Effects Of Intraventricular Angmentioning

confidence: 99%

Section: Cardiovascular Effects Of Intraventricular Angmentioning

confidence: 99%

See 1 more Smart Citation

Angiotensin and baroreflex control of the circulation

Head¹,

Saigusa

Mayorov³

2002

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…An intracerebroventricular (ICV) catheter (Plastics One, Roanoke, VA) was first implanted into the lateral ventricle (coordinates from bregma; 3-mm lateral and 4-mm ventral), 1 week before starting allocated diets, as described previously. 13 Secondly, a recording electrode was implanted on the left renal nerve for the recording of RSNA 14 1 week before the first experiment.…”

Section: Experimental Procedures and Protocolmentioning

confidence: 99%

Obesity-Related Hypertension and the Role of Insulin and Leptin in High-Fat–Fed Rabbits

2013

View full text Add to dashboard Cite

O besity is now a large-scale global epidemic that develops from a complex interaction between genotype and environment, including social, behavioral, cultural, physiological, and metabolic factors. 1 The consequences of being overweight or obese include increased incidence of hypertension, hyperlipidemia and hyperinsulinemia, insulin resistance, and diabetes mellitus.2 Clinical evidence suggests that sympathetic activation participates not only in the initial elevation in blood pressure but also in maintaining the hypertension.3 Obesity is closely linked to increased sympathetic nerve activity (SNA) to the kidneys and skeletal muscle vasculature and is linked to the accumulation of body fat. 4 Our focus has been on the mechanism underlying the increase in blood pressure and, in particular, the role of the sympathetic nervous system in the development of the hypertensive state. We have demonstrated that 3 weeks of high-fat diet (HFD) feeding leads to increased mean arterial pressure (MAP), heart rate (HR), and renal SNA (RSNA) in rabbits. 5 Importantly, we have shown that ganglion blockade completely abolishes the increase in blood pressure suggesting that this model of obesity hypertension is neurogenic. 6 We suggested that the mechanism of the hypertension involved sympathetic activation and increased responsiveness to central sympathoexcitatory effects of leptin owing to increased plasma leptin arising from visceral fat accumulation. 5,6 Leptin is an adipokine that plays an important role in regulating energy intake and energy expenditure, including appetite and metabolism, and acts as a key peripheral hormone in distinct neurons in the hypothalamus.7 Leptin is secreted primarily by adipocytes and is present in serum in direct proportion to the amount of adipose tissue.8 Chronic leptin infusion has been shown to increase HR and blood pressure in animal models 9,10 via stimulation of the sympathetic nervous system. 9,11 In addition to the rise in leptin, we also observed a marked increase in plasma insulin in rabbits fed a HFD suggesting that insulin may also contribute to the hypertension and increased RSNA in rabbits particularly early in the onset of the HFD before significant accumulation of visceral fat. 5,6 Thus, both leptin and insulin may contribute to the hypertension, and with the development of specific antagonists it is now possible to determine their relative roles. In the present study, we administered either the insulin receptor antagonist or the leptin receptor antagonist intracerebroventricularly to conscious rabbits at 1 or 3 weeks after the onset of a HFD. Materials and MethodsTwenty-seven male New Zealand White rabbits (initial body weight, 2.6-3.1 kg) were housed under controlled light (lights on 6:00 Abstract-Feeding a high-fat diet (HFD) to rabbits results in increased blood pressure and renal sympathetic nerve activity (RSNA) and marked increases in plasma leptin and insulin. We determined the contribution of insulin and leptin signaling in the central nervous system to the increased bl...

show abstract

“…Consistent with this, intracisternal administration of angiotensin II, in contrast to intracereboventricular administration, acts mainly on neurons in the brain stem. 34 In the medulla, neurons in the RPa and RVLM are likely sites of action of 8-OH-DPAT. RPa neurons mediate the tachycardia, increased BAT sympathetic activity, and increased cutaneous sympathetic activity that can be evoked by activation of the DMH.…”

Section: Horiuchi Et Al Dmh Cardiovascular Response and 5-ht 1a Recepmentioning

confidence: 99%

Activation of 5-Hydroxytryptamine 1A Receptors Suppresses the Cardiovascular Response Evoked From the Dorsomedial Hypothalamic Nucleus

2005

View full text Add to dashboard Cite

Abstract-The dorsomedial hypothalamic nucleus is a key component of the central pathways subserving the cardiovascular response to psychological stress, which is believed to be an important risk factor for hypertension. Previous studies indicate that 5-hydroxytryptamine 1A receptors can modulate the cardiovascular responses associated with stress. In this study, we determined in anesthetized rats the effects of systemic or intracisternal administration of 8-hydroxy-2-(di-npropylamino)tetralin, a selective agonist of 5-hydroxytryptamine 1A receptors, and then subsequent administration of the selective antagonist WAY-100635 on the cardiovascular response evoked by activation of the dorsomedial hypothalamic nucleus (by microinjection of bicuculline). The increase in mean arterial pressure, heart rate, and renal sympathetic nerve activity (RSNA) evoked by bicuculline injection into the dorsomedial hypothalamic nucleus was greatly reduced (by 80% to 90%) by administration of 8-hydroxy-2-(di-n-propylamino)tetralin and then completely restored by subsequent administration of WAY-100635, whether administered systemically or intracisternally. In contrast, systemic administration of 8-hydroxy-2-(di-n-propylamino)tetralin had no significant effect on the baseline level or reflex changes in RSNA evoked by chemoreceptor or baroreceptor stimulation and resulted in only a modest reduction ( Key Words: Ⅲ hypothalamus Ⅲ stress Ⅲ baroreflex Ⅲ chemoreceptors P sychological stress is believed to be an important risk factor for hypertension and other cardiovascular disorders. 1 Studies in conscious and anesthetized rats have demonstrated that the dorsomedial hypothalamic nucleus (DMH) plays a critical role in mediating the autonomic, neuroendocrine, and behavioral response to psychological stress, such as air jet stress. 2 Activation of neurons in the DMH evokes anxiety-like behavior associated with a wide range of autonomic and hormonal responses, including increases in heart rate (HR; mediated via an increase in cardiac sympathetic nerve activity 3,4 ), renal sympathetic nerve activity (RSNA), gastrointestinal motility, and in the secretion of adrenomedullary hormones and adrenocorticotropic hormone (corticotropin [ACTH]). 2-8 Conversely, bilateral microinjections into the DMH of muscimol (a ␥-aminobutyric acid type A [GABA A ] receptor agonist) or of kynunerate (an antagonist of ionotropic glutamate receptors) greatly reduces the increases in arterial pressure, HR, ACTH secretion, and anxiety-like behavior normally evoked by air jet stress. 8 -10 It has been shown recently that the DMH also plays an important role in generating thermoregulatory responses.Activation of neurons in the DMH evokes an increase in the activity of sympathetic nerves innervating brown adipose tissue (BAT), accompanied by increases in BAT temperature and end-tidal CO 2 , 3 as well as cutaneous vasoconstriction. 11 These thermoregulatory effects may also be part of a stress response because an increase in body temperature can be induced by stress (so-cal...

show abstract

Hemodynamic effects of central angiotensin I, II, and III in conscious rabbits

Cited by 27 publications

References 22 publications

Angiotensin and baroreflex control of the circulation

Angiotensin and baroreflex control of the circulation

Obesity-Related Hypertension and the Role of Insulin and Leptin in High-Fat–Fed Rabbits

Activation of 5-Hydroxytryptamine 1A Receptors Suppresses the Cardiovascular Response Evoked From the Dorsomedial Hypothalamic Nucleus

Contact Info

Product

Resources

About