Reflex release of vasopressin and renin in hemorrhage is enhanced by autonomic blockade

Oliver, James M.; Korner, Paul I.; Woods, Robyn L.; Zhu, Jia L.

doi:10.1152/ajpheart.1990.258.1.h221

Cited by 39 publications

(49 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Plasma renin activity (PRA) was measured via radioimmunoassay, as previously described. 17 At the end of the experiment, the left kidney was weighed. The stage of the estrus cycle of each female rat was also identified by a vaginal smear test and uterine weights were measured at the completion of the experiment.…”

Section: Protocol 1: the Effect Of At 2 R Blockade On Pressure-natriumentioning

confidence: 99%

Gender Differences in Pressure-Natriuresis and Renal Autoregulation

et al. 2011

View full text Add to dashboard Cite

Abstract-Sexual dimorphism in arterial pressure regulation has been observed in humans and animal models. The mechanisms underlying this gender difference are not fully known. Previous studies in rats have shown that females excrete more salt than males at a similar arterial pressure. The renin-angiotensin system is a powerful regulator of arterial pressure and body fluid volume. This study examined the role of the angiotensin type 2 receptor (AT 2 R) in pressure-natriuresis in male and female rats because AT 2 R expression has been reported to be enhanced in females.Renal function was examined at renal perfusion pressures of 120, 100, and 80 mm Hg in vehicle-treated and AT 2 R antagonist-treated (PD123319; 1 mg/kg/h) groups. The pressure-natriuresis relationship was gender-dependent such that it was shifted upward in female vs male rats (PϽ0.001). AT 2 R blockade modulated the pressure-natriuresis relationship, shifting the curve downward in male (PϽ0.01) and female (PϽ0.01) rats to a similar extent. In females, AT 2 R blockade also reduced the lower end of the autoregulatory range of renal blood flow (PϽ0.05) and glomerular filtration rate (PϽ0.01). Subsequently, the renal blood flow response to graded angiotensin II infusion was also measured with and without AT 2 R blockade. We found that AT 2 R blockade enhanced the renal vasoconstrictor response to angiotensin II in females but not in males (PϽ0.05). In conclusion, the AT 2 R modulates pressure-natriuresis, allowing the same level of sodium to be excreted at a lower pressure in both genders. However, a gender-specific role for the AT 2 R in renal autoregulation was evident in females, which may be a direct vascular AT 2 R effect. (Hypertension. 2011;57:275-282.)Key Words: angiotensin type 2 receptor Ⅲ gender differences Ⅲ hypertension Ⅲ natriuresis Ⅲ renal blood flow Ⅲ sodium I t is well-established that women are protected from cardiovascular and renal disease relative to men before menopause. 1 However, the mechanisms responsible for this gender difference are poorly understood, partly because females remain underrepresented in human clinical trials and animal studies. 2,3 Evidence suggests that estrogen plays a protective role against cardiovascular disease in women, 4 and previous studies have identified gender differences in the activity of the renin-angiotensin system (RAS), 1 a major regulator of arterial pressure.Studies in rodents have also revealed major gender differences in the expression of RAS components and differences in the way males and females respond to stimulation and inhibition of the RAS under physiological and pathophysiological circumstances. [5][6][7][8] Recently, with the discovery of angiotensin-converting enzyme 2, a depressor axis to the RAS has been identified 9 that incorporates the angiotensin type 2 receptor (AT 2 R), which is upregulated by estrogen. 7,10 Previously, we have demonstrated that the vasodepressor RAS pathways are enhanced in females and that the AT 2 R has a depressor influence on the response to chronic ang...

show abstract

Section: Protocol 1: the Effect Of At 2 R Blockade On Pressure-natriumentioning

confidence: 99%

Gender Differences in Pressure-Natriuresis and Renal Autoregulation

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Resting mean ear arterial pressure (MAP) was measured for 1 hour, and arterial blood (1 mL) was collected for plasma renin activity (PRA) determination. 18 Rabbits were then randomized to 4 groups. Under halothane anesthesia, a clip was placed around the left (nϭ7) or right (nϭ7) renal artery, 6 an osmotic minipump (Alzet 2ML4, Durect; replaced 22 days later under local analgesia) was inserted subcutaneously for delivery of Ang II (20 to 50 ng kg Ϫ1 min Ϫ1 , Auspep; nϭ9), or sham surgery was performed (nϭ8).…”

Section: Animals and Experimental Designmentioning

confidence: 99%

Renal Sympathetic Neuroeffector Function in Renovascular and Angiotensin II–Dependent Hypertension in Rabbits

et al. 2007

View full text Add to dashboard Cite

Abstract-We tested the hypotheses that the gains of specific renal sympathetic neuroeffector mechanisms are altered in secondary hypertension and that the nature of these alterations depends on the precise experimental setting of the kidney. Rabbits were sham operated, or made comparably hypertensive (mean arterial pressure increased 17% to 24%) by clipping the left or right renal artery or by chronic infusion of angiotensin II (20 to 50 ng kg Ϫ1 min Ϫ1 SC). Four to 6 weeks later, under pentobarbital anesthesia, the left renal nerves were sectioned and electrically stimulated at low (0 to 2 Hz) and high (4 to 8 Hz) frequencies. Neurally evoked reductions in total renal blood flow, cortical perfusion, urine flow, and sodium excretion and increases in renal norepinephrine spillover were not significantly greater in kidneys of hypertensive rabbits than normotensive controls. Neurally evoked increases in renal renin release and the slope of the relationship between renin release and norepinephrine spillover were less in kidneys of hypertensive rabbits than normotensive controls. Low-frequency renal nerve stimulation reduced medullary perfusion, which was negatively correlated with renal norepinephrine spillover in kidneys from all 3 groups of hypertensive rabbits but not normotensive controls. Two-hertz stimulation reduced medullary perfusion by 19% in hypertensive rabbits but not in normotensive rabbits. Thus, of all of the renal sympathetic neuroeffector mechanisms studied, only neural control of medullary perfusion was enhanced in these models of secondary hypertension. This effect appears to be mediated postjunctionally, not through enhanced neural norepinephrine release, and may contribute to the development and/or maintenance of hypertension in these models. Key Words: kidney circulation Ⅲ renal medulla Ⅲ renal sympathetic nerves Ⅲ renin-angiotensin system Ⅲ sodium excretion T he renal sympathetic nerves appear to contribute to the pathogenesis of essential hypertension. Human essential hypertension is accompanied by increased sympathetic nerve activity, including to the kidney, and defects in neuronal norepinephrine uptake. 1 Renal sympathetic nerve activity (RSNA) is greater in spontaneously hypertensive rats than in normotensive rats, and renal denervation delays or blunts the development of hypertension in spontaneously hypertensive rats. 2 The role of the sympathetic nervous system in secondary hypertension remains controversial. Sympathetic vasomotor drive may be increased in hypertension induced by chronic infusion of angiotensin II (Ang II; Ang II-induced hypertension) 3-5 and in 2 kidney, 1 clip (2K1C) hypertension, 6,7 because depressor responses to sympatholysis or ganglionic blockade are augmented. Furthermore, muscle SNA and total norepinephrine spillover are increased in human renovascular hypertension. 8 Renal denervation can delay or blunt 2K1C and Ang II-induced hypertension, 9 -11 suggesting a contribution of increased RSNA or increased renal responsiveness to RSNA. However, RSNA is not neces...

show abstract

“…On day 0, mean arterial pressure (MAP) and body weight were measured in rabbits, and blood was collected (1.5 mL) to measure hematocrit and plasma renin activity (PRA). 9 Surgery was then performed to induce 2-kidney, 1-wrapped (2K,1W) Page hypertension (nϭ7; meanϮSEM age, 4.3Ϯ0.5 months; meanϮSEM weight, 3.2Ϯ0.1 kg). The control group underwent a sham operation (nϭ5; meanϮSEM age, 4.3Ϯ0.9 months; meanϮSEM weight, 3.2Ϯ0.2 kg).…”

Section: Mothersmentioning

confidence: 99%

Adult Rabbit Offspring of Mothers With Secondary Hypertension Have Increased Blood Pressure

et al. 2003

View full text Add to dashboard Cite

Abstract-Preexisting chronic hypertension complicates up to 5% of pregnancies and is associated with an increased risk of low-birth-weight babies. Studies suggest that an adverse intrauterine environment leading to low birth weight is linked to an increased risk of cardiovascular disease, including hypertension, in the adult. In this study, the blood pressure of offspring from mothers with hypertension were followed up into adulthood. Two-kidney, 1-wrapped hypertension was induced in 7 female rabbits; 5 other rabbits underwent sham surgery. Four weeks later, rabbits were mated, at which time mean arterial pressure was 118Ϯ3 and 87Ϯ5 mm Hg in the hypertensive and sham groups, respectively (PϽ0.001). The blood pressure of 30-week-old females was 89Ϯ2 mm Hg in the offspring of hypertensive (nϭ14) and 79Ϯ1 mm Hg in the offspring of normotensive (nϭ13) mothers (PϽ0.005). Also, plasma renin activity was significantly lower in the female offspring of hypertensive mothers at 10 weeks of age (PϽ0.05), suggesting that development of the renin-angiotensin system was altered. In contrast, male offspring from hypertensive and normotensive mothers had similar mean arterial pressure and plasma renin activity. In conclusion, maternal secondary hypertension can "program" hypertension in female adult offspring. The results also suggest that there are gender-specific differences in sensitivity to altered in utero environmental influences. Key Words: blood pressure Ⅲ rabbits Ⅲ hypertension, secondary Ⅲ pregnancy Ⅲ renin Ⅲ gender H ypertension is the most common complication associated with pregnancy. 1 Preexisting chronic hypertension complicates up to 5% of pregnancies and is associated with an increased risk of preterm labor, uteroplacental insufficiency, placental detachment, and low birth weight. 2,3 In the United States, the percentage of mothers older than 30 years increased from 16% in 1976 to 37% in 2001 4,5 ; it is also known that the rate of hypertension increases in women Ͼ30 years of age. 6 It is therefore predicted that the incidence of chronic hypertension during pregnancy will increase in association with this trend toward childbearing at older ages. Epidemiological studies suggest that an adverse intrauterine environment leading to low birth weight is linked to an increased risk of cardiovascular disease, including hypertension, in the adult. 7,8 Even mild chronic hypertension during pregnancy has been associated with low birth weight. 2,3 We have therefore investigated the effect of chronic hypertension during pregnancy on the blood pressure of adult offspring. To this end, secondary hypertension was induced in female rabbits, these rabbits were mated, and then the blood pressure of their offspring was followed up into adulthood. The adult offspring were also subjected to the prohypertensive physiological challenges of an increased salt diet and weight gain.

show abstract

Reflex release of vasopressin and renin in hemorrhage is enhanced by autonomic blockade

Cited by 39 publications

References 0 publications

Gender Differences in Pressure-Natriuresis and Renal Autoregulation

Gender Differences in Pressure-Natriuresis and Renal Autoregulation

Renal Sympathetic Neuroeffector Function in Renovascular and Angiotensin II–Dependent Hypertension in Rabbits

Adult Rabbit Offspring of Mothers With Secondary Hypertension Have Increased Blood Pressure

Contact Info

Product

Resources

About