Differences In Utero in Activities of Catecholamine Biosynthetic Enzymes in Adrenals of Spontaneously Hypertensive Rats

1981 ◽  
Vol 61 (s7) ◽  
pp. 227s-230s ◽  
Author(s):  
G. Teitelman ◽  
R. A. Ross ◽  
T. H. Joh ◽  
D. J. Reis

1. We sought to determine if catecholamine biosynthetic enzymes of spontaneously hypertensive rats (SHR) differed from those of normotensive Wistar—Kyoto (WKY) and Sprague—Dawley (SD) control rats before birth. 2. By immunocytochemical and biochemical methods we compared strains for the time of appearance and maturation of the enzymes tyrosine hydroylase (TH), dopamine-β-hydroxylase (DBH) and phenylethanolamine-N-methyltransferase (PNMT) in sympathetic ganglia and adrenals. 3. The time of appearance of enzymes was identical in all three strains: TH and DBH first appeared in sympathetic ganglia on embryonic day 11 (E11) and in adrenal medulla on E16. PNMT, restricted to adrenal medulla, appeared later on E18. 4. The activity of adrenal TH prenatally on E18 and E21 and at day of birth (P1) in SHR was approximately two fold that in WKY or SD rats. In contrast PNMT was lower in SHR but only on E18. 5. Thus, although the timing of the first expression of adrenergic phenotypes is similar in SHR and normotensive controls, the differences in TH activity in adrenals suggest an enhanced biosynthetic capacity for catecholamines in this strain before birth. 6. We conclude that SHR differ from normotensive rats from the first expression of some of the genes controlling catecholamine biosynthesis.

1995 ◽  
Vol 6 (4) ◽  
pp. 1209-1215
Author(s):  
Q C Meng ◽  
J Durand ◽  
Y F Chen ◽  
S Oparil

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.


1995 ◽  
Vol 268 (4) ◽  
pp. H1549-H1554 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall

Previous studies from this laboratory demonstrated that there was enhanced basal and evoked (K+ depolarization) overflow of endogenous norepinephrine (NE) into the perfusate of a push-pull cannula placed in the paraventricular nucleus of the hypothalamus (PVH) of conscious freely moving spontaneously hypertensive rat (SHR) compared with Wistar-Kyoto (WKY) or Sprague-Dawley (SD) rats. The present study was carried out to determine whether results obtained with SHR were specific to this genetic model of hypertension by examining NE release in deoxycorticosterone acetate (DOCA)-salt hypertension. DOCA-salt hypertension was produced in 8-wk-old uninephrectomized SD rats by administering a 50-mg DOCA Silastic pellet subcutaneously 7 days postnephrectomy and providing 0.9% NaCl + 0.2% KCl drinking solution at libitum for 3 wk. Sham-implanted animals received normal tap water. Blood pressure was similar to that of 8- to 10-wk-old SHR. Basal release of NE as well as release after K+ added to the push-pull cannula or sodium nitroprusside or phenylphrine administered intravenously was determined. It was observed that there was no difference in basal overflow or after K+ administration in DOCA-salt hypertensive rats compared with sham animals. Similarly, the increase in NE overflow due to sodium nitroprusside or the decrease due to phenylphrine was similar between DOCA-salt rats or sham controls. This was in sharp contrast to what was observed in SHR: basal or K(+)-evoked release was significantly greater in SHR than WKY, SD, DOCA-salt, or DOCA-sham controls. It is concluded that central noradrenergic activity involving the PVH is not altered in DOCA-salt hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Vol 59 (11) ◽  
pp. 1111-1116 ◽  
Author(s):  
Gary L. Wright

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.


1986 ◽  
Vol 71 (1) ◽  
pp. 121-123 ◽  
Author(s):  
Koh-Ichi Murakawa ◽  
Yoshiharu Kanayama ◽  
Masakazu Kohno ◽  
Takahiko Kawarabayashi ◽  
Kenichi Yasunari ◽  
...  

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.


1979 ◽  
Vol 236 (4) ◽  
pp. H635-H639
Author(s):  
D. S. Chen ◽  
D. E. Donald ◽  
J. C. Romero

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.


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