Vasodepressor Effects of Arachidonic Acid and Prostacyclin (PGI2) in Hypertensive Rats

1981 ◽  
Vol 61 (s7) ◽  
pp. 315s-318s ◽  
Author(s):  
G. J. Dusting ◽  
R. Di Nicolantonio ◽  
T. Drysdale ◽  
A. E. Doyle
Keyword(s):  
Arachidonic Acid ◽  
Renal Hypertension ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Intravenous Injections ◽  
Sprague Dawley Rats ◽  
Experimental Renal Hypertension ◽  
Wistar Kyoto ◽  
High Doses

1. Vasodepressor responses to prostacyclin and nitroprusside were compared in anaesthetized, spontaneously hypertensive rats of the Okamoto strain and Wistar—Kyoto controls, and also in one-kidney, one-clip hypertensive rats and unilaterally nephrectomized controls of the Sprague—Dawley strain. The responses, measured as a percentage of resting blood pressure, did not differ significantly between the hypertensive rats and the normotensive controls within each strain. 2. The effects of intravenous injections of arachidonic acid were also studied in each strain. 3. The vasodepressor effects of high doses of arachidonic acid (1 or 3 mg/kg) were much greater and more prolonged in both groups of hypertensive rats. These differences were abolished by indomethacin (2 mg/kg). 4. Comparisons between the strains showed that whereas Okamoto rats have significantly greater depressor responsiveness to nitroprusside and prostacyclin than Sprague—Dawley rats, the depressor effects of high doses of arachidonic acid (1 and 3 mg/kg) were smaller in the normotensive Wistar-Kyoto than in the Sprague—Dawley rats. 5. It is concluded that hypertensive rats have enhanced ability to transform exogenous arachidonic acid into vasodilator prostanoids. This occurs both in spontaneous hypertension and in experimental renal hypertension. However, rats of the Okamoto strain appear to have reduced ability to form prostacyclin when compared with Sprague—Dawley rats.

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.

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.

Neuropeptide action in nucleus tractus solitarius: angiotensin specificity and hypertensive rats

1985 ◽  
Vol 249 (3) ◽  
pp. R341-R347 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Heart Rate ◽  
Nucleus Tractus Solitarius ◽  
Dose Range ◽  
Cardiovascular Effects ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

We have reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius of urethan-anesthetized normotensive rats produces an increase in mean arterial pressure (MAP) over the dose range 50-500 pmol. The effect in spontaneously hypertensive rats (SHR) is now reported. Over the range 100-500 pmol SHR exhibit increases in MAP and heart rate greater than Wistar-Kyoto or Sprague-Dawley rats. SHR did not exhibit exaggerated responses to intravenous phenylephrine, suggesting a central site of increased responsiveness to ANG II. We also found depressor effects in Sprague-Dawley at lower doses (0.1 and 1 pmol). The decreases in MAP were extremely variable and not dose related. A selected dose of additional neuropeptides identified in the NTS was tested. Somatostatin, bradykinin, and vasoactive intestinal peptide (0.5 nmol) were without cardiovascular effects. Oxytocin and vasopressin, however, produced significant increases in MAP. Substance P produced a very small but significant increase in heart rate and MAP. Interaction between the vasopressin and ANG II pressor effects was studied, and each proved to be independent.

Abnormal magnesium metabolism in two rat models of genetic hypertension

1992 ◽  
Vol 70 (9) ◽  
pp. 1225-1229 ◽  
Author(s):  
I. C. Wells ◽  
D. K. Agrawal
Keyword(s):  
Tap Water ◽  
Mesenteric Arteries ◽  
Magnesium Concentration ◽  
Erythrocyte Ghosts ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Control Value ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

Magnesium concentrations in erythrocyte ghosts and arterial tissue of male, spontaneously hypertensive rats (SHR) were significantly less than in these tissues of male normotensive controls (Wistar–Kyoto; WKY) of the same age, which were also fed rat chow and tap water. The magnesium concentration in SHR erythrocyte ghosts was increased to the control value by incubating SHR erythrocytes with WKY blood plasma; SHR plasma did not affect the magnesium concentration in WKY erythrocyte ghosts. The magnesium concentrations in erythrocyte ghosts, aortas, and mesenteric arteries from female salt-sensitive (SS/JR) and salt-resistant (SR/JR) Dahl-derived rats, both maintained ad libitum on laboratory rat chow and either tap water or 0.9% NaCl, were not different but were significantly less than those of Sprague–Dawley rats considered as controls. While the ingestion of 0.9% NaCl had no effect on the magnesium concentrations measured in these animals, it caused the salt-sensitive rats to become severely hypertensive. It is evident from these observations that the decreased binding of magnesium to the plasma membrane of cells may be an inheritable metabolic defect that may be associated with the development of hypertension. However, in those instances of hypertension in which this defect occurs, it appears to be a contributing cause of the hypertension; by itself the defect is not a cause of hypertension.Key words: essential hypertension, magnesium, SHR rats, salt-sensitive rats (SS/JR).

High-NaCl diets increase natriuretic and diuretic responses in salt-resistant but not salt-sensitive SHR

1991 ◽  
Vol 260 (6) ◽  
pp. F890-F897 ◽  
Author(s):  
M. S. Mozaffari ◽  
S. Jirakulsomchok ◽  
Z. H. Shao ◽  
J. M. Wyss
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Isotonic Saline ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Volume Loading ◽  
Spontaneously Hypertensive ◽  
Volume Load ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study tested the hypothesis that NaCl-sensitive spontaneously hypertensive rats (SHR-S) display a defect in natriuretic and diuretic responses to acute volume loading that contributes to the rise in arterial pressure observed when the rats are fed a high-NaCl diet. Seven-week-old SHR-S and NaCl-resistant SHR rats (SHR-R) and normotensive (Wistar-Kyoto and Sprague-Dawley rats) were fed high- or basal NaCl diets. After 2.5 wk on the diets, preinstrumented conscious rats received an intravenous infusion (5% body wt; 0.5 ml/min) of isotonic saline, and urine was collected through a bladder catheter for 90 min. Control rats on the high-NaCl diet (compared with basal) excreted a significantly greater percentage of Na+ and volume load. In contrast, SHR-S on high-NaCl diet (compared with basal) had a very small increase in natriuretic response and no increase in diuretic response to volume expansion. The effect of renal denervation on natriuretic and diuretic responses to volume load was tested. In SHR-R on 1 and 8% NaCl diets, renal denervation had little or no effect on these responses, suggesting that renal nerves do not play a prominent role in the dietary NaCl-induced increases in the natriuretic and diuretic responses to volume load. These results demonstrate that NaCl-resistant rats rapidly adapt to diets high in NaCl content with increased natriuretic and diuretic responses to acute volume loading. The failure of SHR-S to adapt to the dietary challenge may result in volume loading and a secondary increase in arterial pressure after feeding.

Aortic Reactivity of Rats with Genetic and Experimental Renal Hypertension

1972 ◽  
Vol 50 (11) ◽  
pp. 1072-1079 ◽  
Author(s):  
F. P. Field ◽  
R. A. Janis ◽  
D. J. Triggle
Keyword(s):  
Smooth Muscle ◽  
Renal Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Aortic Smooth Muscle ◽  
Low Concentrations ◽  
Experimental Renal Hypertension ◽  
Altered Cell ◽  
Specific Alteration ◽  
Spontaneous Contractions

The isometric tensions produced by low concentrations of norepinephrine (1 × 10−10 and 3 × 10−10M) or potassium (10 mM) were greater in aortic rings from mature rats with hypertension produced by bilateral renal encapsulation and from rats with genetic hypertension than from Car-worth normotensive Wistar rats. This hyper-reactivity was not associated with a hypersensitivity to low calcium concentrations in the presence of 80 mM KCl. Similarly the loss of maximum response to KCl with time in calcium-free solution was the same for aortic smooth muscle from normotensive and hypertensive rats. However, the rate of relaxation after 80 mM KCl was washed from the bath with normal Krebs solution was much faster for aortic smooth muscle from normotensive than from hypertensive animals. Spontaneous contractions were observed in aortic rings obtained from eight of 12 renal hypertensive rats but were not observed in rings from either spontaneously hypertensive or normotensive rats. An elevated thyroid activity was not associated with the increase in systolic blood pressure to 185 mm Hg in the renal encapsulated rats. The results suggest that the hypersensitivity to norepinephrine of the aortic smooth muscle is due to an altered cell membrane rather than a specific alteration of the adrenergic α-receptors.

Age-dependent overflow of endogenous norepinephrine from paraventricular hypothalamic nucleus of hypertensive rats

1993 ◽  
Vol 265 (1) ◽  
pp. H39-H46 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall
Keyword(s):  
Blood Pressure ◽  
Neuronal Activity ◽  
Reciprocal Relationship ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Paraventricular Hypothalamic Nucleus ◽  
Wistar Kyoto ◽  
The Relationship

The relationship between age and central noradrenergic neuronal activity of the paraventricular hypothalamic nucleus (PVH) was examined in 7- to 10-, 12- to 14-, and 30- to 36-wk-old Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR). As an index of noradrenergic activity, endogenous norepinephrine (NE) overflow was assessed utilizing a miniaturized push-pull cannula assembly in unanesthetized freely moving rats. NE overlow under basal, 56 mM K+ stimulation, and in response to pressor/depressor drugs, were examined in all three strains at all ages. Significant increases in basal and K(+)-stimulated overflow of endogenous NE from the PVH were observed in all ages of SHR compared with normotensive controls with the greatest percent increase occurring during the development of hypertension in SHR. In addition, a reciprocal relationship exists with respect to blood pressure and overflow of NE from the PVH such that increases/decreases in blood pressure elicit decreases/increases in NE overflow in all strains at all ages examined. However, developing hypertensive SHR exhibited attenuated decreases in overflow of NE from the PVH compared with age-matched controls and established hypertensive SHR. These results suggest that noradrenergic pathways of the PVH contribute to the development and maintenance of arterial pressure hemostasis and that enhanced central noradrenergic neuronal activity is greatest during the development of hypertension in SHR.

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