Vascular prostaglandin synthesis in the spontaneously hypertensive rat

1977 ◽  
Vol 233 (4) ◽  
pp. H493-H499 ◽  
Author(s):  
C. J. Limas ◽  
C. Limas
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Inferior Vena ◽  
Spontaneously Hypertensive Rat ◽  
Vena Cava ◽  
Prostaglandin Synthesis ◽  
Hypertensive Rats ◽  
Blood Pressure Elevation ◽  
Spontaneously Hypertensive ◽  
Prostaglandin Dehydrogenase ◽  
Wistar Kyoto

Vascular prostaglandin synthesis was studied in tissues (aorta and inferior vena cava) obtained from spontaneously hypertensive rats (SHRs) of the Aoki-Okamoto strain and age-matched Wistar-Kyoto (WKYs) controls. PGE2 synthesis in aortas from SHRs was significantly enhanced at 10 wk of age (5.3 +/- 0.7 nmol PGE2/mg protein per 10 min vs. 1.9 +/- 0.03 nmol PGE2/mg protein per min in the WKYs, P less than 0.001) and increased progressively until 22 wk of age; PGE2alpha synthesis in SHRs was not significantly different from WKYs. In the venous walls from SHRs, PGF2alpha was the prostaglandin predominantly synthesized (7.1 +/- 0.6 vs. 1.9 +/- 0.05 nmol PGE2alpha/mg protein per 10 min in the WKY controls, P less than 0.01). The activities of 15-hydroxy prostaglandin dehydrogenase and PGE 9-ketoreductase were also compared in the two groups of animals. The only difference detected was a significant increase in venous PGE 9-ketoreductase of SHR's (7.3 +/- 0.06 vs. 4.8 +/- 0.04 nmol PGF2alpha/mg per min, P less than 0.01). The results suggest that increased vascular synthesis of prostaglandins accompanies the development of spontaneous hypertension and may serve to attenuate the effects of blood pressure elevation.

Mechanism of exaggerated diuresis in spontaneously hypertensive rats

1978 ◽  
Vol 235 (5) ◽  
pp. F409-F416 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Rios
Keyword(s):  
Volume Expansion ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Nephron ◽  
Wistar Kyoto

The mechanism of exaggerated diuresis and natriuresis was studied in spontaneously hypertensive rats (SHR) by renal clearance and micropuncture techniques. Control normotensive rats of the same age and sex [Wistar-Kyoto rats (WKY)] were also studied. During the hydropenic control and the volume-expansion experimental periods absolute and fractional water and sodium excretion were greater in SHR than in WKY. Although fractional and absolute water and sodium reabsorption were similar along the proximal convolution in SHR and WKY, fractional and absolute water reabsorption in Henle's loop was less in SHR than in WKY. Hydrostatic and colloid osmotic pressures in the cortical peritubular microvasculature were similar in WKY and SHR. Acute normalization of renal perfusion pressure by aortic constriction reversed the exaggerated diuresis and natriuresis in SHR by halving the filtered load of water and sodium; whole kidney and single nephron glomerular filtration rates and blood flows decreased by 50%. It is concluded that the exaggerated diuresis and natriuresis of the spontaneously hypertensive rat is caused by a decreased reabsorption in the loop of Henle. The mechanism of this decreased reabsorption in the loop of Henle cannot be explained by alterations in the measured physical forces in the renal cortical microvasculature. natriuresis; autoregulation; volume expansion Submitted on November 15, 1977 Accepted on June 7, 1978

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.

Trace elements during the development of hypertension in the spontaneously hypertensive rat

1987 ◽  
Vol 72 (4) ◽  
pp. 515-518 ◽  
Author(s):  
A. Berthelot ◽  
C. Luthringer ◽  
A. Exinger
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Concentrations ◽  
Total Plasma ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
X Ray ◽  
Spectrometry Technique ◽  
Trace Element Levels ◽  
Wistar Kyoto

1. Total plasma concentrations of bromine, copper, rubidium, selenium and zinc were measured in spontaneously hypertensive rats (SHR) and Wistar–Kyoto rats (WKY) of 5–20 weeks of age, using an X-ray fluorescence spectrometry technique. 2. Although plasma levels of bromine, rubidium, selenium and zinc varied at different ages when comparing SHR and WKY, their general evolution was similar. Copper levels increased more in SHR than in WKY. 3. These perturbations in trace element levels could perhaps participate in the establishment of hypertension in SHR, but could also be due to genetic differences between the strains, unrelated to the development of hypertension.

Cell Membrane Microviscosity and Ca2+-Mg2+-ATPase Activity do Not Contribute to Hypertension in the Spontaneously Hypertensive Rat Model

1993 ◽  
Vol 85 (5) ◽  
pp. 585-591 ◽  
Author(s):  
Robert I Norman ◽  
Navtej Achall
Keyword(s):  
Blood Pressure ◽  
Atpase Activity ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Membrane Microviscosity ◽  
Spontaneously Hypertensive ◽  
Blood Pressures ◽  
Wistar Kyoto ◽  
Spontaneously Hypertensive Rat Model

1. The relationships between systolic blood pressure and altered erythrocyte Ca2+-Mg2+-ATPase activity and membrane microviscosity were assessed in membranes prepared from 20-week-old female Wistar-Kyoto normotensive and spontaneously hypertensive rats obtained from two different sources (Charles River and Harlan OLAC) and a second filial (F2) generation derived from a cross between Wistar-Kyoto rats and spontaneously hypertensive rats from one source (Charles River). 2. Spontaneously hypertensive rats from both sources had systolic blood pressures significantly higher than those of Wistar-Kyoto animals (P <0.05; 151 + 4 and 110 + 3 mmHg, Charles River; 155 + 4 and 122 + 4 mmHg, Harlan OLAC). The systolic blood pressures for the F2 rat population ranged between 73 and 168 mmHg. 3. Ca2+-Mg2+-ATPase activity was measured as ATP-dependent 45Ca2+ uptake into inside-out vesicles and microviscosity assessed by the measurement of polarization anisotropy of membrane incorporated fluorescent probes including 1,6-diphenyl-1,3,5-hexatriene, trimethylamino-1,6-diphenyl-1,3,5-hexatriene and a series of anthroyloxy fatty acids. 4. Contrary to previous studies, no relationship between adult systolic blood pressure and erythrocyte Ca2+-Mg2+-ATPase activity or general or localized membrane microviscosity was indicated by the comparison of spontaneously hypertensive and Wistar-Kyoto animals or in the analysis of the F2 rat population. 5. These results suggest that Ca2+-Mg2+-ATPase activity and membrane microviscosity are causally unrelated to hypertension in these animals. On the assumption that biophysical properties of the erythrocyte membrane reflect those of smooth muscle, our results suggest that membrane alteration does not play a significant role in the pathogenesis of hypertension in the spontaneously hypertensive rat model.

Prolonged isobaric relaxation time in small mesenteric arteries of the spontaneously hypertensive rat

1987 ◽  
Vol 65 (2) ◽  
pp. 230-235 ◽  
Author(s):  
C. Subah Packer ◽  
Newman L. Stephens
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Relaxation Times ◽  
Peripheral Resistance ◽  
Mesenteric Arteries ◽  
Relaxation Rates ◽  
Resistance Arteries ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Prolonged isometric relaxation in hypertensive aortic and caudal arterial smooth muscle has been demonstrated; however, isobaric relaxation in resistance arteries is more pertinent to studies in hypertension. A comparative study of mesenteric arterial isobaric relaxation times was made using spontaneously hypertensive rats (SHR), normotensive Wistar–Kyoto rats (WKY), and MK-421 treated SHR (treatment commenced at 8 weeks of age and was maintained until sacrifice). Relaxation rates of vessels constricting against a range of pressures and achieving different degrees of narrowing or changes in circumference were analyzed. Comparisons were made between SHR, WKY, and MK-421 treated SHR arteries that had constricted from the same initial circumference and against the same magnitude of pressure. The SHR mesenteric arteries relaxed at a slower rate than did the WKY vessels. The normotensive MK-421 treated SHR showed the same prolonged relaxation rate as did the untreated SHR preparations. Thus the slower rate of relaxation in SHR arteries does not appear to be a consequence of the hypertension. Such prolonged time for narrowing would function to increase the average peripheral resistance and thus may contribute to the initiation and maintenance of increased blood pressure.

Renin Response to Volume Contraction and Indomethacin in Spontaneously Hypertensive Rats

1981 ◽  
Vol 60 (5) ◽  
pp. 479-482 ◽  
Author(s):  
J. L. Cangiano ◽  
Carmen Rodriguez-Sargent ◽  
L. Nascimento ◽  
M. Martinez-Maldonado
Keyword(s):  
Sharp Increase ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Prostaglandin Synthesis ◽  
Restricted Diet ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Volume Contraction ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Wistar Kyoto

1. The effects of volume contraction and indomethacin on renin response were examined in spontaneously hypertensive rats and Wistar-Kyoto normotensive rats. Volume contraction was induced by frusemide or by salt-restricted diet combined with frusemide administration. 2. Plasma renin levels were not altered by either procedure in spontaneously hypertensive rats (5.2 ± 0.8 versus 5.6 ± 0.9 ng h−1 ml−1). Normotensive rats responded to volume contraction with a sharp increase in plasma renin activity (13.1 ± 1.2 to 23.3 ± 1.1 ng h−1 ml−1). 3. Intraperitoneal injection of indomethacin for 1 week did not alter basal renin levels in either group. In contrast, indomethacin pretreatment caused renin to rise in response to frusemide in spontaneously hypertensive rats (4.7 ± 0.8 to 27.1 ± 1.8 ng h−1 ml−1). 4. These findings suggest that a prostaglandin normally inhibits the renin response of spontaneously hypertensive rats to frusemide-induced volume contraction. Inhibition of prostaglandin synthesis allows volume contraction to stimulate renin release.

Upregulation of endothelin-1 binding in tissues of salt-loaded stroke-prone spontaneously hypertensive rats

2002 ◽  
Vol 80 (5) ◽  
pp. 470-474 ◽  
Author(s):  
Paula Savage ◽  
Arco Y Jeng
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Similar Proportion ◽  
Receptor Subtypes ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Endothelin 1 ◽  
Wistar Kyoto ◽  
Kidney Liver ◽  
The Brain

Upon maintained on a 1% NaCl drinking solution beginning at 7 weeks of age, the stroke-prone spontaneously hypertensive rat (SHRsp) developed severe hypertension and stroke; most died by 16 weeks. The mechanism by which these diseases evolve remains unclear. Endothelin-1 (ET-1) is a potent, peptidic vasoconstrictor and is implicated in the pathogenesis of various cardiovascular, renal, and central nervous system diseases. The purpose of the present study was to compare the binding of [125I]ET-1 to the brain, heart, kidney, liver, and spleen membrane preparations of 16-week-old SHRsp and age-matched normotensive Wistar–Kyoto rats (WKY). The KD values for [125I]ET-1 binding to the corresponding tissues of the two strains were not significantly different, except in the brain (SHRsp: 17 ± 1 pM; WKY: 24 ± 1 pM). In contrast, the Bmax values measured in the brain, heart, kidney, and liver of SHRsp were 1.5- to 2.1-fold greater than those of their WKY counterparts. Competition of [125I]ET-1 binding to the membrane preparations by the specific ETA receptor antagonist BQ-123 or the specific ETB receptor agonist sarafotoxin S6c revealed a similar proportion of ETA and ETB receptor subtypes in the corresponding tissues of the two rat strains. These results indicate that ET-1 binding is upregulated in SHRsp and suggest that ET-1 may play a pathophysiological role in this animal model of genetic hypertension.Key words: ETA receptor, ETB receptor, BQ-123, sarafotoxin 6C, stroke-prone spontaneously hypertensive rats.

Factors producing elevated core temperature in spontaneously hypertensive rats

1987 ◽  
Vol 63 (2) ◽  
pp. 740-745 ◽  
Author(s):  
M. G. Collins ◽  
W. S. Hunter ◽  
C. M. Blatteis
Keyword(s):  
Core Temperature ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Thermal Conductance ◽  
Evaporative Heat Loss ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ambient Temperatures ◽  
Metabolic Heat ◽  
Wistar Kyoto

Core temperature (Tco) of the spontaneously hypertensive rat (SHR) is consistently higher by approximately 1 degree C than that of normotensive controls. To analyze factors producing the elevated Tco, mean skin temperature (Tsk), metabolic heat production (M), respiratory evaporative heat loss (Eres), effective tissue thermal conductance (K), systolic blood pressure (BP), and Tco were determined in eight male SHR and nine male normotensive Wistar-Kyoto (WKY) rats habituated to rest quietly in neck stock restraint while exposed to ambient temperatures (Ta) of 12.5, 17, 23, 28.5, 32, 34, and 35 degrees C. At all temperatures steady-state BP, Tco, and M were higher for SHR's than for WKY's. SHR's could maintain thermal balance up to Ta 32 degrees C, and WKY's up to 34 degrees C. Eres from SHR's was greater than from WKY's at Ta of 12.5, 17, and 28.5 degrees C. K of SHR's was not different from or was higher than K of WKY's, and K for both groups was 2.6 times greater at Ta 32 degrees C than at 17 degrees C. These results indicate that the high Tco of SHR's is due to increased M uncompensated by increased K or Eres.

Increased Presynaptic α-Adrenoceptor-Mediated Regulation of Noradrenaline Release in the Isolated Perfused Kidney of Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 309s-311s ◽  
Author(s):  
R. D. Ekas ◽  
M. L. Steenberg ◽  
M. F. Lokhandwala
Keyword(s):  
Nerve Stimulation ◽  
Noradrenaline Release ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Isolated Perfused Kidney ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Hypertensive Rat ◽  
Wistar Kyoto

1. Release of [3H]noradrenaline during peri-arterial nerve stimulation and its inhibition by the presynaptic α-adrenoceptor mechanism were studied in the isolated perfused kidney from spontaneously hypertensive and Wistar-Kyoto rats. 2. A frequency related vasoconstriction as well as [3H]noradrenaline release were observed over the stimulating range of 0.25-32 Hz in both the Wistar-Kyoto and spontaneously hypertensive rats. The spontaneously hypertensive rat kidneys exhibited both an increased vasoconstrictor response and a greater [3H]noradrenaline release when compared with the Wistar-Kyoto rat kidneys. 3. Presynaptic inhibition of [3H]noradrenaline release was evaluated at 2 Hz by using the α-adrenoceptor agonist, tramazoline. Increasing concentrations of tramazoline from 2 × 10−9 mol/l to 2 × 10−7 mol/l caused a dose-dependent decrease in the stimulus-induced release of [3H]noradrenaline in spontaneously hypertensive rats but not in Wistar-Kyoto rats. Only 2 × 10−7 mol/l tramazoline had an inhibitory effect in the Wistar-Kyoto rats. 4. These data indicate that noradrenaline release during sympathetic nerve stimulation is greater in the spontaneously hypertensive rat. The supersensitivity of presynaptic α-adrenoceptors observed in spontaneously hypertensive rats may be a consequence of the greater noradrenaline release present in these animals.

Corticosterone 6 beta-hydroxylation correlates with blood pressure in spontaneously hypertensive rats

1992 ◽  
Vol 262 (6) ◽  
pp. F927-F931 ◽  
Author(s):  
C. O. Watlington ◽  
L. B. Kramer ◽  
E. G. Schuetz ◽  
J. Zilai ◽  
W. M. Grogan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Selective Inhibitor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Human Hypertension ◽  
Before And After ◽  
Wistar Kyoto ◽  
Cytochrome P 450

Evidence for increased glucocorticoid 6 beta-hydroxylation (enhanced family 3A cytochrome P-450 activity) is found in certain reversible forms of human hypertension. This association was investigated in the spontaneously hypertensive rat (SHR). The proportion of injected [3H]corticosterone excreted in urine as 6 beta-[3H]OH-corticosterone was four- to fivefold higher in SHR than in control Wistar-Kyoto rats, before and after development of overt hypertension. Both hypertension and 6 beta-hydroxylation were inhibited by troleandomycin (a selective inhibitor of family 3A cytochromes P-450), consistent with a role for increased steroid 6 beta-hydroxylation in the genesis of hypertension in the SHR.

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