Modulation of Sympathetic Vascular Tone by Prostaglandins in Corticosterone-Induced Hypertension in Rats

1979 ◽  
Vol 57 (s5) ◽  
pp. 235s-237s ◽  
Author(s):  
W. Rascher ◽  
R. Dietz ◽  
A. Schömig ◽  
G. Burkart ◽  
J. B. Lüth ◽  
...  

1. In corticosterone-induced hypertension in rats the activity of the peripheral sympathetic nervous system and its modulation by prostaglandins was studied. 2. Plasma concentrations of noradrenaline were reduced if compared with those in normotensive control rats. 3. The sensitivity of the isolated perfused hindlimb preparation to noradrenaline was enhanced before blood pressure rose and increased further with the development of hypertension. 4. Arachidonic acid, prostacyclin (prostaglandin I2), but not 6-keto-prostaglandin F1α, reversed the supersensitivity to noradrenaline. 5. These results suggest that corticosterone induces a supersensitivity to noradrenaline by inhibiting the biosynthesis of prostaglandins. Changes in the sensitivity of the vascular smooth muscle may play a role in the development of glucocorticoid hypertension.

1983 ◽  
Vol 65 (5) ◽  
pp. 469-474 ◽  
Author(s):  
S. M. Gardiner ◽  
T. Bennett

1. Rats housed individually in glass metabolism cages develop hypertension. Since previous experiments have provided some evidence for the involvement of the sympathetic nervous system in the maintenance of the hypertension, the present work was designed to explore the possible involvement of the sympathetic nervous system in the genesis of isolation-induced hypertension. 2. Male and female Wistar rats were treated neonatally with guanethidine, with a protocol designed to produce an extensive peripheral sympathectomy; control rats received saline. 3. The effects of isolation on systolic blood pressure and fluid and electrolyte balances were studied when the rats were mature. 4. Guanethidine-treated rats did not develop hypertension in response to isolation whereas control rats did. 5. There were no significant differences between the fluid and electrolyte balances of the guanethidine-treated rats compared with controls throughout the period of isolation. 6. It is concluded that a fully functional sympathetic nervous system is required for the development of isolation-induced hypertension, but its involvement is not through a modulation of renal function.


Hypertension ◽  
2019 ◽  
Vol 73 (1) ◽  
pp. 162-170 ◽  
Author(s):  
Frank T. Spradley ◽  
Ana C. Palei ◽  
Christopher D. Anderson ◽  
Joey P. Granger

Preeclampsia is a pregnancy-specific disorder of new-onset hypertension linked to placental ischemia. While obesity is a major risk factor for preeclampsia, not all obese pregnant women develop pregnancy-induced hypertension or preeclampsia. Previously, we reported that placental ischemia-induced hypertension is dependent upon intact signaling of the sympathetic nervous system. Moreover, in various models of obesity, blockade of MC4R (melanocortin-4 receptor) signaling protects against the development of hypertension via suppression of the sympathetic nervous system. Less is known about this pathway during obese pregnancy. Although blockade of MC4R may lead to increased body weight during pregnancy, we tested the hypothesis that placental ischemia-induced hypertension is attenuated in obese MC4R-deficient pregnant rats. On gestational day 14, MC4R wild-type or heterozygous-deficient (MC4R-def) rats were subjected to chronic placental ischemia via the reduced uterine perfusion pressure procedure or Sham surgery then examined on gestational day 19. In Sham MC4R-def versus Sham wild-type pregnant rats, there was increased body weight, fat mass, and circulating leptin levels but they had similar fetus weights. Reduced uterine perfusion pressure reduced fetus weights in both strains. Reduced uterine perfusion pressure increased blood pressure in wild-type rats but this response was significantly attenuated in MC4R-def rats, although blood pressure was elevated in Sham MC4R-def over Sham wild-type. These data indicate that while obese MC4R-def pregnant rats have higher blood pressure during pregnancy, placental ischemia-induced hypertension is attenuated in obese MC4R-def pregnant rats. Thus, obese women with abnormal MC4R signaling may be less susceptible to the development of placental ischemia-induced hypertension.


1986 ◽  
Vol 71 (1) ◽  
pp. 111-115 ◽  
Author(s):  
Peter C. Rubin ◽  
Lucy Butters ◽  
Rosemary McCabe ◽  
John L. Reed

1. Increased activity of the sympathetic nervous system has been implicated in the genesis of early hypertension in young people. Studies in pregnancy allow observations to be made on evolving, recently established and resolving hypertension in the human. We describe the results of two studies involving women who developed hypertension during pregnancy. 2. In the first study, plasma concentrations of noradrenaline and adrenaline were measured in 17 women with pregnancy induced hypertension (PIH) and 17 normotensive pregnant control subjects. Plasma noradrenaline (nmol/l) was lower in the PIH group compared with control patients in both semi-recumbent (1.11 ± 0.53 vs 1.98 ± 0.96, P < 0.001) and standing positions (1.31 ± 0.65 vs 2.57 ± 1.27, P < 0.005). Five days post partum, plasma noradrenaline had risen in the PIH group compared with pregnant values in semi-recumbent (1.65 ± 1.0 vs 1.11 ± 0.52, P < 0.05) and standing positions (2.46 ± 1.5 vs 1.31 ± 0.65, P < 0.05). In the normotensive patients plasma noradrenaline did not differ between post partum and pregnant values (1.51 ± 0.73 vs 1.98 ± 0.96 semi-recumbent; 2.00 ± 1.16 vs 2.57 ± 1.7 standing). 3. Logarithmic transformation of the noradrenaline concentration data resulted in a significant (P < 0.02) negative correlation with diastolic blood pressure in the pregnant patients but not post partum. Plasma adrenaline concentration was the same in both groups. 4. In the second study, plasma concentrations of noradrenaline and adrenaline were measured sequentially through pregnancy in five women who developed PIH and five control subjects who remained normotensive. There was no difference in catecholamine concentrations between groups at any stage, but noradrenaline concentration tended to fall as blood pressure rose in the PIH patients. 5. We conclude that the sympathetic nervous system does not contribute to the development of PIH but responds to the increased blood pressure with decreased activity.


1986 ◽  
Vol 250 (5) ◽  
pp. R770-R775 ◽  
Author(s):  
J. L. Williams ◽  
M. D. Johnson

Experiments were performed to determine the functional role of the sympathetic nervous system (SNS) in blood pressure regulation in Brattleboro diabetes insipidus (DI) rats and to determine the effects of synthetic arginine vasopressin (AVP) on sympathetic function in DI rats. The experiments were conducted in male age-matched Long-Evans (LE) and DI rats in the conscious unstressed state. Mean arterial pressure (MAP) and heart rate were similar in conscious unstressed LE and DI rats, but basal plasma concentrations of norepinephrine (NE) and epinephrine (E) were elevated in DI rats compared with LE rats. An intra-arterial bolus injection of hexamethonium (30 mg/kg) resulted in greater reductions of MAP in DI rats (-62 +/- 5 mmHg) than in LE rats (-42 +/- 7 mmHg; P less than 0.05). Administration of AVP to DI rats by osmotic minipump reduced plasma NE concentration in DI rats to a level not different from that in LE rats, but E concentration remained elevated. AVP administration to DI rats also reduced the hexamethonium-induced fall in MAP in these animals (-47 +/- 7 mmHg) to a level not different from that in LE rats. We conclude that the SNS plays a greater role in blood pressure maintenance in conscious DI rats than in LE rats and that AVP administration can normalize plasma NE concentration and the contribution of the SNS to blood pressure maintenance in these animals.


1957 ◽  
Vol 188 (2) ◽  
pp. 371-374 ◽  
Author(s):  
Sol Rothman ◽  
Douglas R. Drury

The blood pressure responses to various drugs were investigated in renal hypertensive, cerebral hypertensive and normotensive rabbits. Hexamethonium bromide and Dibenamine reduced the blood pressures of renal and cerebral hypertensives. Effects in the normal were insignificant. The cerebral hypertensive's blood pressure was slightly affected by benzodioxane. Blood pressure was not reduced at all in the other groups. Blood pressure of the renal hypertensive rabbit was greatly reduced by Veriloid and dihydroergocornine. Blood pressures of cerebral and normal animals were affected to a lesser degree. The results suggest that maintenance of hypertension in the cerebral hypertensive rabbit depends on an overactive sympathetic nervous system, possibly due to the release of medullary pressor centers from inhibitory impulses originating in higher centers; whereas, the maintenance of hypertension in the renal hypertensive rabbit may be attributed to an increased reactivity of the peripheral vasculature to a normal sympathetic tone.


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