Renin-angiotensin, arterial blood pressure, and salt appetite in rats

Thunhorst, Robert L.; Johnson, Alan Kim

doi:10.1152/ajpregu.1994.266.2.r458

Cited by 55 publications

(92 citation statements)

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“…Also, salt appetite is stimulated, not reduced, after administration of a vasodilator (minoxidil) and captopril, which causes a modest decrease in MAP. Finally, the magnitude of the salt appetite is reduced when phenylephrine is used to block the decrease in MAP after injections of furosemide and captopril treatment (43). Thus the small decrease in MAP after intraventricular injection of the V 1 receptor antagonist probably has no role in reducing salt intake by sodium-deficient rats in the present study.…”

Section: Discussionmentioning

confidence: 57%

Brain vasopressin and sodium appetite

Flynn

Kirchner

Clinton

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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ventricular injections of vasopressin (VP) and antagonists with varying degrees of specificity for the VP receptors were used to identify the action of endogenous brain VP on 0.3 M NaCl intake by sodium-deficient rats. Lateral ventricular injections of 100 ng and 1 g VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. 8 ]VP (MeT-AVP) significantly suppressed NaCl intake by sodium-deficient rats without causing motor disturbances. MeT-AVP had no effect on sucrose intake (0.1 M). In contrast, the selective V2 receptor antagonist had no significant effect on NaCl intake. Last, injections of 100 ng MeT-AVP decreased mean arterial blood pressure (MAP), whereas 100 ng VP elevated MAP and pretreatment with MeT-AVP blocked the pressor effect of VP. These results indicate that the effects produced by 100 ng MeT-AVP represent receptor antagonistic activity. These findings suggest that the effect of exogenous VP on salt intake is secondary to motor disruptions and that endogenous brain VP neurotransmission acting at V1 receptors plays a role in the arousal of salt appetite. neurohypophysial peptides; taste; blood pressure; V 1 receptor; V2 receptor VASOPRESSIN (VP) has diverse biological actions and target systems. In addition to the well-known neuroendocrine effects, VP meets the criteria for a brain neurotransmitter. For example, it is synthesized in several brain nuclei, including the paraventricular nucleus of the hypothalamus, medial amygdala, and bed nucleus of the stria terminalis (1, 5). Also, physiological stimuli trigger the release of VP in specific brain regions where it exerts its effects on pre-and postsynaptic membranes (11, 31).VP exerts its effects through receptors that have been divided into two broad classes, the V 1 and V 2 receptors. The V 1 class can be further divided into the V 1a and V 1b receptors (16,17,42). The receptors differ in their distribution and associated second messenger system (17). Neurons that synthesize VP have extensive vasopressinergic projections to sites along the neuraxis, including the septum, hippocampus, amygdala, subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), nucleus of the solitary tract, dorsal motor nucleus of the vagus, and spinal cord (1,29,40). Radioligand receptor autoradiography and in situ hybridization results indicate that VP binding sites are distributed in the brain and that the distribution of these sites often overlaps with the terminal distributions of vasopressinergic neurons (22,32,46).Brain release and pituitary release of VP often parallel one another. For example, systemic osmotic and hypovolemic stimuli that increase circulating VP levels also stimulate the release of VP in the lateral septum and lateral ventricle (4). Manipulations that facilitate salt intake can also stimulate the systemic release of VP. The simultaneous administration of furosemide and a low dose of the angiotensin-converting enzyme captopril arouses a sodium appetite and increases ...

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Section: Discussionmentioning

confidence: 57%

Brain vasopressin and sodium appetite

Flynn

Kirchner

Clinton

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Salt appetite is satisfied by ingesting Na but not chloride (Rowland et al, 2004). In experimental conditions, systemic administrations of diuretic agents such as furosemide and of colloids such as polyethylene glycol have been reported to induce salt intake behavior only for several hours (Thunhorst and Johnson, 1994). During the loss of body salt, natriorexigenic hormones and mineralocorticoid hormones are secreted from peripheral tissues, and they stimulate salt-intake behavior and renal reabsorption of Na + (Fitzsmons, 1998).…”

Section: General Introduction Thirst and Salt Appetite Are Controlledmentioning

confidence: 99%

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

et al. 2016

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“…Isoproterenol injection does not induce sodium intake (32) despite the high levels of ANG II and the hypotension that have been implicated in mediating salt appetite (6,26,33). However, in rats injected with methysergide into the LPBN, sc isoproterenol elicits ingestion of a significant amount of 0.3 M NaCl, which suggests that any activation of sodium intake produced by isoproterenol is strongly inhibited by inhibitory mechanisms that have LPBN as a relay (11).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, the aim of the present study was to investigate the effects of electrolytic lesion of the commNTS on water and 0.3 M NaCl intake after subcutaneous injection of isoproterenol, a drug that activates the renin-angiotensin system (9). Since isoproterenol induces hypotension, and this can facilitate water and sodium intake (22,26), we also evaluated the effects of isoproterenol on blood pressure in comm-NTS-lesioned rats.…”

Section: Introductionmentioning

confidence: 99%

Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

Blanch

Freiria-Oliveira

Colombari

et al. 2007

Braz J Med Biol Res

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The nucleus of the solitary tract (NTS) is the primary site of the cardiovascular afferent information about arterial blood pressure and volume. The NTS projects to areas in the central nervous system involved in cardiovascular regulation and hydroelectrolyte balance, such as the anteroventral third ventricle region and the lateral parabrachial nucleus. The aim of the present study was to investigate the effects of electrolytic lesion of the commissural NTS on water and 0.3 M NaCl intake and the cardiovascular responses to subcutaneous injection of isoproterenol. Male Holtzman rats weighing 280 to 320 g were submitted to sham lesion or electrolytic lesion of the commissural NTS (N = 6-15/group). The sham-lesioned rats had the electrode placed along the same coordinates, except that no current was passed. Water intake induced by subcutaneous isoproterenol (30 µg/kg body weight) significantly increased in chronic (15 days) commissural NTS-lesioned rats (to 2.4 ± 0.2 vs sham: 1.9 ± 0.2 mL 100 g body weight -1 60 min -1 ). Isoproterenol did not induce any sodium intake in sham or in commissural NTS-lesioned rats. The isoproterenol-induced hypotension (sham: -27 ± 4 vs commissural NTS-lesioned rats: -22 ± 4 mmHg/20 min) and tachycardia (sham: 168 ± 10 vs commissural NTS: 144 ± 24 bpm/20 min) were not different between groups. The present results suggest that the commissural NTS is part of an inhibitory neural pathway involved in the control of water intake induced by subcutaneous isoproterenol, and that the overdrinking observed in lesioned rats is not the result of a cardiovascular imbalance in these animals.

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Renin-angiotensin, arterial blood pressure, and salt appetite in rats

Cited by 55 publications

References 0 publications

Brain vasopressin and sodium appetite

Brain vasopressin and sodium appetite

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

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