Effect of pinealectomy on arterial blood pressure and food and water intake in the rat

1978 ◽  
Vol 1 (2) ◽  
pp. 125-130 ◽  
Author(s):  
A. Zanoboni ◽  
A. Forni ◽  
W. Zanoboni-Muciaccia ◽  
C. Zanussi
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Arterial Blood ◽  
Food And Water Intake

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Hemodynamic, hormonal, and drinking responses to reduced venous return in the dog

1982 ◽  
Vol 243 (3) ◽  
pp. R354-R362 ◽  
Author(s):  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Venous Return ◽  
Control Level ◽  
Vena Cava ◽  
Plasma Renin ◽  
Ang Ii ◽  
Arterial Blood ◽  
Dog Plasma

The effect of an acute reduction in venous return, caused by reversible constriction of the thoracic vena cava, on drinking and secretion or arginine vasopressin (AVP) was examined in the dog. Plasma AVP levels rose immediately from a control level of 1.4 +/- 0.1 pg/ml (mean +/- SE) to a plateau ranging between 36 and 42 pg/ml during the first 30 min after constriction but declined to 12.6 +/- 4.2 pg/ml 2 h after constriction even though systemic arterial hypotension was maintained. Drinking occurred with a latency of 22 +/- 6 min and 13.2 +/- 1.8 ml H2O/kg was consumed during 2 h of vena caval constriction. Water intake was significantly correlated with the average reduction in blood pressure (r = 0.86; n = 8; P less than 0.01) but not with plasma renin activity. The role of angiotensin II (ANG II) in the drinking and secretion of AVP in response to decreased venous return was evaluated using the ANG II receptor blocker, saralasin, infused intravenously (iv) or intracerebroventricularly (icv). Intravenous, but not icv, infusion of saralasin during vena caval constriction reduced the ability of the dogs to maintain arterial blood pressure (P less than 0.05). However, neither iv nor icv saralasin significantly affected water intake or the rise in plasma AVP in response to vena caval constriction when compared to their respective controls. Taken together, these data show that angiotensin is important in the maintenance of systemic arterial blood pressure but is not essential for the rise in plasma AVP or drinking in response to an acute reduction in venous return. It is suggested that either arterial baroreceptors or "low-pressure" volume receptors or both mediate the drinking and AVP responses in the presence of central blockade of the effects of circulating angiotensin.

Abstract 017: Optogenetic Activation of OVLT Neurons Stimulates Water Intake and Produces a Sympathetically-Mediated Increase in Arterial Blood Pressure

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sean D Stocker ◽  
Sarah S Simmonds
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Body Fluid ◽  
Frequency Dependent ◽  
Fluid Homeostasis ◽  
Direct Activation ◽  
Arterial Blood ◽  
Body Fluid Homeostasis

The organum vasculosum of the lamina terminalis (OVLT) plays a pivotal role in body fluid homeostasis and arterial blood pressure (ABP) regulation. The OVLT lacks a complete blood-brain-barrier and responds to an array of circulating factors such as NaCl and angiotensin II. Lesion of the anteroventral third ventricular region which includes the OVLT attenuates or reverses several forms of salt-sensitive hypertension. However, there is limited evidence to demonstrate that direct activation of OVLT neurons alters body fluid homeostasis or elevates ABP. To address this question, Male-Sprague-Dawley rats (300-350 g) received an injection of rAAV9-CamKII-hChR2(H134R)-EYFP (10 12 particles/mL, 200nL) into the OVLT. A fiber optic cannula (200μm) was implanted 300μm dorsal to OVLT. Approximately 2-3 week later, optogenetic activation of OVLT neurons (10ms pulse, 50% duty cycle, 30 min) produced frequency-dependent increases in water intake (1Hz: 1.0±0.5mL; 5Hz: 4.2±0.6mL; 10Hz: 8.0±1.8; 20Hz: 10.2±2.1mL, n=4, P<0.05). In separate experiments, optogenetic activation of OVLT neurons produced a frequency-dependent increase in mean ABP (1Hz: 1±1 mmHg; 5Hz: 3±1mmHg; 10Hz: 7±1mmHg; 20Hz: 13±1mmHg, n=4, P<0.05) and heart rate (1Hz: 3±6 bpm; 5Hz: 15±5bpm; 10Hz: 40±12 bpm; 20Hz: 62±14bpm, n=4, P<0.05). Pretreatment with the vasopressin antagonist Manning Compound (10ug/kg, IV) did not affect these responses. However, pretreatment with the ganglionic blocker chlorisondamine (5mg/kg, IV) abolished the pressor (20Hz: 1±1 mmHg, P<0.01) and tachycardic (20Hz: 4±7 bpm, P<0.05) responses to activation of OVLT neurons. Finally, in vivo single-unit recordings demonstrate that optogenetic activation produced frequency-dependent increases in cell discharge of OVLT neurons responsive to either intracarotid injection of hypertonic NaCl (0.3M NaCl, 50μL over 10 s, n=6) or angiotensin II (100ng over 10s, n=3). Collectively, these data provide evidence that direct activation of OVLT neurons stimulates thirst and produces a sympathetically-mediated increase in ABP.

Deletion of cyclooxygenase-2 in the mouse increases arterial blood pressure with no impairment in renal NO production in response to chronic high salt intake

2013 ◽  
Vol 304 (10) ◽  
pp. R899-R907 ◽  
Author(s):  
Mette Stæhr ◽  
Pernille B. L. Hansen ◽  
Kirsten Madsen ◽  
Paul M. Vanhoutte ◽  
Rolf M. Nüsing ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Salt Intake ◽  
High Salt ◽  
No Production ◽  
Arterial Blood ◽  
High Salt Intake ◽  
Cox 2

Experiments were designed to test the hypothesis that cyclooxygenase-2 (COX-2) activity attenuates the blood pressure increase during high NaCl intake by stimulation of endothelial nitric oxide synthase (eNOS)-mediated NO synthesis in the kidney medulla. COX-2−/− (C57BL6) an COX-2+/+ mice were fed a diet with 0.004% (low salt, LS) or 4% (high salt, HS) NaCl for 18 days. Arterial blood pressure was recorded continuously using indwelling catheters. Food and water intake and diuresis were measured in metabolic cages. Urine osmolality and excretion of electrolytes, cGMP, cAMP, and NOx were determined, as well as plasma NOx and cGMP. There was a significant dependence of blood pressure on salt intake and genotype: COX-2−/− exhibited higher blood pressure than COX-2+/+ both on HS and LS intake. COX-2+/+ littermates displayed an increase in blood pressure on HS versus LS (102.3 ± 1.1 mmHg vs. 91.9 ± 0.9 mmHg) day and night. The mice exhibited significant blood pressure increases during the awake phase (night) that were larger in COX-2−/− on HS diet compared with COX-2+/+. Water intake, diuresis, Na+, and osmolyte excretions and NOx and cGMP excretions were significantly and similarly elevated with HS in COX-2−/− and COX-2+/+. In summary, C57BL6 mice exhibit a salt intake-dependent increase in arterial blood pressure with increased renal NO production. COX-2 activity has a general lowering effect on arterial blood pressure. COX-2 dampens NaCl-induced increases in arterial blood pressure in the awake phase. In conclusion, COX-2 activity attenuates the changes in nocturnal blood pressure during high salt intake, and COX-2 activity is not necessary for increased renal nitric oxide formation during elevated NaCl intake.

Sign in / Sign up

Export Citation Format

Share Document