GABA-A Agonist Muscimol Inhibits Stimulated Vasopressin Release in the Posterior Pituitary of Sprague-Dawley, Wistar, Wistar-Kyoto and Spontaneously Hypertensive Rats

1993 ◽  
Vol 58 (5) ◽  
pp. 519-524 ◽  
Author(s):  
Åsa M. Magnusson ◽  
Bengt J. Meyerson
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Posterior Pituitary ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Vasopressin Release ◽  
Gaba A ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Methionine-enkephalin and vasopressin in SHR: effects of dehydration

1986 ◽  
Vol 250 (6) ◽  
pp. R1007-R1013
Author(s):  
K. Ota ◽  
L. Share ◽  
J. T. Crofton ◽  
D. P. Brooks
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Posterior Pituitary ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Wistar Kyoto ◽  
Shr And Wky Rats

Enkephalins are found in the posterior pituitary, can alter vasopressin secretion, and have greater pressor effects in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto (WKY) rats. Measurement of the plasma methionine-enkephalin concentration (PMet-Enk) has provided equivocal results in humans and has not been reported in rats. We have developed a highly specific and sensitive Met-Enk radioimmunoassay and determined that Met-Enk circulates in rats but that PMet-Enk is no different between SHR and WKY rats (7.6 +/- 0.8 and 9.2 +/- 0.8 pg/ml, respectively). Water deprivation for 48 h increased the plasma vasopressin concentration (PADH) and 24-h urinary vasopressin excretion (UADHV) in SHR and WKY rats, but PMet-Enk was not altered. There were no differences in PADH and UADHV between SHR and WKY rats in either the euhydrated or dehydrated state. These results suggest that it is unlikely that circulating Met-Enk contributes importantly to the maintenance of hypertension in SHR. There was also no evidence for a greater secretion of vasopressin in SHR than in WKY rats, in contrast to previous reports.

scholarly journals Effects of dietary salt on angiotensin peptides in kidney.

1995 ◽  
Vol 6 (4) ◽  
pp. 1209-1215
Author(s):  
Q C Meng ◽  
J Durand ◽  
Y F Chen ◽  
S Oparil
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Angiotensin Peptides ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.

scholarly journals Ganglionic Long-Term Potentiation in Prehypertensive and Hypertensive Stages of Spontaneously Hypertensive Rats Depends on GABA Modulation

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Luis A. Martínez ◽  
Fredy Cifuentes ◽  
Miguel A. Morales
Keyword(s):  
Synaptic Plasticity ◽  
Spontaneously Hypertensive Rats ◽  
Long Term Potentiation ◽  
Hypertensive Rats ◽  
Gaba A ◽  
Spontaneously Hypertensive ◽  
Term Potentiation ◽  
Cervical Ganglia ◽  
Wistar Kyoto

The sympathetic nervous system (SNS) regulates body functions in normal and pathological conditions and is characterized by the presence of a neuroplastic phenomenon, termed ganglionic long-term potentiation (gLTP). In hypertension, either in spontaneously hypertensive rats (SHR) or in humans, sympathetic hyperfunction, such as elevated SNS outflow and changes in synaptic plasticity have been described. Because enhanced SNS outflow is detected in the hypertensive stage and, more importantly, in the prehypertensive phase of SHR, here we explored whether synaptic plasticity, particularly gLTP, was modified in the superior cervical ganglia (SCG) of prehypertensive SHR. Furthermore, considering that GABA modulates sympathetic synaptic transmission and gLTP in Wistar rats, we studied whether GABA might modulate gLTP expression in SHR. We characterized gLTP in the SCG of young prehypertensive 6-week-old (wo) and adult hypertensive (12 wo) SHR and in the SCG of Wistar Kyoto (WKy) normotensive control rats of the same ages. We found that gLTP was expressed in 6 wo SHR, but not in 12 wo rats. By contrast, in WKy, gLTP was expressed in 12 wo, but not in 6 wo rats. We also found that gLTP depends on GABA modulation, as blockade of GABA-A subtype receptors with its antagonist bicuculline unmasked gLTP expression in adult SHR and young WKy. We propose that (1) activity-dependent changes in synaptic efficacy are altered not only during hypertension but also before its onset and (2) GABA may play a modulatory role in the changes in synaptic plasticity in SHR, because the blockade of GABA-A receptors unmasked the expression of gLTP. These early changes in neuroplasticity and GABA modulation of gLTP could be part of the sympathetic hyperfunction observed in hypertension.

The vascular sensitizing character of plasma from spontaneously hypertensive rats

1981 ◽  
Vol 59 (11) ◽  
pp. 1111-1116 ◽  
Author(s):  
Gary L. Wright
Keyword(s):  
Blood Pressure ◽  
Plasma Levels ◽  
Spontaneously Hypertensive Rats ◽  
Vascular Tissue ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tissue Sensitivity ◽  
Low Levels ◽  
Wistar Kyoto

Experiments were conducted to examine the effects of plasma from spontaneously hypertensive rats (systolic blood pressure (SBP) = 183 torr; 1 torr = 133.322 Pa) on the contractile properties of aortic strips from normotensive rats. While incubated in plasma from spontaneously hypertensive (SH) rats, the aortic strips of normotensive rats exhibited hyperresponsiveness to norepinephrine (NE) compared with those incubated in plasma obtained from Wistar–Kyoto (SBP = 128 torr) or Sprague–Dawley (SBP = 110 torr) rats. The washout of plasma and perfusion of the aortic strips with Krebs bicarbonate solution abolished the effect of SH plasma on the reactivity to NE but not potassium, suggesting a residual hypersensitivity. The comparison of these findings with results obtained for contractions of aortic strips in Krebs bicarbonate solution containing high and low levels of calcium indicated the effect of SH plasma on vascular tissue sensitivity was not directly related to an alteration in plasma levels of calcium.

Cytoplasmic free [Ca2+] is not increased in the platelets of deoxycorticosterone–salt and spontaneously hypertensive rats

1986 ◽  
Vol 71 (1) ◽  
pp. 121-123 ◽  
Author(s):  
Koh-Ichi Murakawa ◽  
Yoshiharu Kanayama ◽  
Masakazu Kohno ◽  
Takahiko Kawarabayashi ◽  
Kenichi Yasunari ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Free Calcium ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Acetoxymethyl Ester ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Significant Difference ◽  
Free Calcium Concentration ◽  
Wistar Kyoto

1. The cytoplasmic free calcium concentration ([Ca2+]i) in the platelets of spontaneously hypertensive rats (SHR), Wistar–Kyoto rats (WKY), deoxycorticosterone–salt hypertensive rats (DOC) and normotensive Sprague–Dawley rats (SD) was measured with the fluorescent dye, quin-2-tetra-acetoxymethyl ester. 2. No significant difference in platelet [Ca2+]i was found between SHR and WKY or between DOC and SD rats. 3. No correlations were found between systolic blood pressure and [Ca2+]i. 4. These results suggest that the elevation of platelet [Ca2+]i does not necessarily accompany hypertension in rats.

Role of vagal afferents in vasodepressor effects of PGE2 in spontaneously hypertensive rats

1979 ◽  
Vol 236 (4) ◽  
pp. H635-H639
Author(s):  
D. S. Chen ◽  
D. E. Donald ◽  
J. C. Romero
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Jugular Vein ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cervical Vagotomy ◽  
Wistar Kyoto ◽  
Cardiopulmonary Receptors ◽  
Depressor Effect

In anesthetized, spontaneously hypertensive rats (Okamoto-Aoki), injections of 0.75, 1.5, and 3.0 microgram/kg PGE2 into the jugular vein caused transient decreases (mean +/- SE) in arterial pressure of 21 +/- 2, 37 +/- 3, and 78 +/- 6 mmHg, respectively, before cervical vagotomy and of 1 +/- 1, 15 +/- 4, and 15 +/- 6 mmHg after cervical vagotomy. The vasodepressor effect of jugular vein injections of 3.0 microgram/kg PGE2, but not of lower doses, was depressed by vagotomy in normotensive Wistar-Kyoto and Sprague-Dawley rats. Vagotomy did not reduce the hypotensive response to intra-aortic injections of PGE2 in these hypertensive and normotensive rats. The depressor effect of PGE2 thus appears to have a significant reflex component mediated through cardiopulmonary receptors subserved by vagal afferents, with hypertensive rats exhibiting a lower threshold than normotensive rats. A vagally mediated reflex component to the depressor effect of PGE2 could not be demonstrated in normotensive rabbits or in rabbits and rats with chronic renovascular hypertension. Thus, a naturally occurring vasoactive substance can stimulate cardiopulmonary receptors subserved by vagal afferents in the rat, and spontaneously hypertensive rats appear to be especially sensitive to this effect.

Decreased in vitro responses to vasoconstrictors during gestation in normotensive and spontaneously hypertensive rats

1987 ◽  
Vol 65 (12) ◽  
pp. 2466-2471 ◽  
Author(s):  
G. Massicotte ◽  
J. St-Louis ◽  
A. Parent ◽  
E. L. Schiffrin
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Female Rats ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Pregnant Rats ◽  
Spontaneously Hypertensive ◽  
Vasoconstrictor Agents ◽  
Wistar Kyoto

We have investigated the in vitro vascular responses to vasoconstrictor agents in pregnant normotensive (Sprague–Dawley (SDR) and Wistar–Kyoto (WKR)) and spontaneously hypertensive rats (SHR) to measure the sensitivity and contractility of blood vessels of pregnant rats. In the perfused mesenteric vascular bed from rats on the 21st day of gestation, the concentration–response curves for the increase in perfusion pressure by arginine8-vasopressin and norepinephrine were displaced to the right by comparison to nonpregnant female rats when all strains of rats were considered together. The increase in EC50 to both agents in pregnant rats was from 1.3- to 2.7-fold in the mesenteric bed; SDR showed the highest increase in EC50, followed by SHR and WKR. No consistent effect was observed on the maximum response. Similar results were obtained in isolated portal veins for angiotensin II and norepinephrine, except that the increase in EC50 in pregnant rats was smaller in magnitude (from 1.0 to 1.7) and followed the same interstrain pattern. These data show that the decreased responsiveness to vasoconstrictor agents in pregnant rats observed in vitro is similar in normotensive and hypertensive rats and suggest that the factor(s) responsible for this effect is a phenomenon affecting vascular smooth muscle in both arteries and veins.

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