Pineal Hyperactivity in Spontaneously Hypertensive Rats: Muscarinic Regulation of Indole Metabolism

1990 ◽  
Vol 79 (5) ◽  
pp. 437-442 ◽  
Author(s):  
Liliana M. E. Finocchiaro ◽  
Angelika Scheucher ◽  
Azucena L. Alvarez ◽  
Samuel Finkielman ◽  
Victor E. Nahmod ◽  
...  
Keyword(s):  
Pineal Gland ◽  
Binding Sites ◽  
Spontaneously Hypertensive Rats ◽  
Electrical Field Stimulation ◽  
Metabolic Effects ◽  
Hypertensive Rats ◽  
Electrical Field ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. Choline acetyltransferase activity and [3H]quinuclidinyl benzylate-binding sites were detected in the pineal gland of normotensive Wistar—Kyoto rats and of spontaneously hypertensive rats. 2. In vitro, muscarinic activation by pilocarpine increased the pineal metabolic production of hydroxyindole derivatives up to 5-hydroxytryptamine and produced a less marked stimulation of melatonin biosynthesis. 3. Electrical field stimulation of pineal gland slices caused similar metabolic effects. 4. Muscarinic blockade with atropine inhibited the effects on hydroxyindole metabolism. 5. [3H]Quinuclidinyl benzylate-binding sites, indicative of muscarinic receptors, were more numerous, and basal 5-hydroxytryptamine and melatonin levels were higher, in the pineal gland of spontaneously hypertensive rats compared with Wistar—Kyoto rats. 6. The atropine-sensitive metabolic effects of pilocarpine and electrical field stimulation on the pineal gland were increased in spontaneously hypertensive rats compared with Wistar-Kyoto rats.

Carvacrol Improves Erectile Dysfunction in Spontaneously Hypertensive Rats

2019 ◽  
Author(s):  
Tays Gonçalves ◽  
Priscilla Maciel ◽  
Larissa Villanueva ◽  
Pablo Santos ◽  
Ismael Oliveira Junior ◽  
...  
Keyword(s):  
Erectile Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
Pressure Ratio ◽  
Electrical Field Stimulation ◽  
Hypertensive Rats ◽  
Electrical Field ◽  
Spontaneously Hypertensive ◽  
Corpora Cavernosa ◽  
Relaxation Responses ◽  
Wistar Kyoto

Carvacrol is a monoterpene found in essential oils from various plants. Several pharmacological properties have already been described for carvacrol, including antimicrobial, anti-inflammatory, anticarcinogenic, antioxidant, vasorelaxant and hypotensive activities. The present study evaluated the effect of carvacrol on hypertensive rats with erectile dysfunction. Twelve-week-old spontaneously hypertensive rats (SHR) were treated with vehicle, carvacrol (50 or 100 mg/kg/day) or sildenafil (1.5 mg/kg/day), intragastrically, for four weeks. Wistar Kyoto (WKY) rats were used as the normotensive controls. All substances tested reduced systolic blood pressure during the treatment period. The intracavernosal pressure/mean arterial pressure ratio of the hypertensive rats was improved by carvacrol and sildenafil treatments. In isolated rat corpora cavernosa, the acetylcholine- and SNP-induced relaxation responses were significantly increased by carvacrol or sildenafil treatments. In SHR corpora cavernosa, treatment with carvacrol attenuated the hypercontractility induced by phenylephrine or electrical field stimulation. Phe-induced hypercontractility in the presence of tempol was not altered when compared to the response induced by carvacrol alone. In rat corpora cavernosa fluorescence intensity emitted by the DHE probe was significantly reduced in SHR treated (carvacrol or sildenafil) groups when compared to that emitted in the SHR-CTL. This study showed that carvacrol improves the erectile function of hypertensive rats and reduces endothelial dysfunction, smooth muscle cell hypercontractility and superoxide anion generation.

Central bradykininergic system in normotensive and hypertensive rats

1992 ◽  
Vol 82 (5) ◽  
pp. 513-519 ◽  
Author(s):  
Azucena L. Alvarez ◽  
Alejandro Delorenzi ◽  
Daniel Santajuliana ◽  
Samuel Finkielman ◽  
Victor E. Nahmod ◽  
...  
Keyword(s):  
Pineal Gland ◽  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Hypertensive Rats ◽  
Kinin System ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Arterial Blood ◽  
Wistar Kyoto ◽  
Dorsal Medulla

1. The kinin antagonist des-Arg9−[Leu8]bradykinin, injected into the lateral ventricle, caused a long-lasting, dose-dependent reduction in arterial blood pressure and heart rate in spontaneously hypertensive rats but not in normotensive Wistar-Kyoto rats; the antagonist also blocked the pressor response to ventricularly infused bradykinin in both strains. 2. Bradykinin content was increased in the hypothalamus and septum and decreased in the dorsal medulla of spontaneously hypertensive rats when compared with those of normotensive Wistar-Kyoto rats, whereas similar bradykinin contents were observed in the pineal gland, hypophysis and rostroventrolateral medulla of both rat strains. 3. Increased concentrations of bradykinin and its precursor kininogen were found in the cerebrospinal fluid of spontaneously hypertensive rats. 4. Bradykinin receptor numbers, measured as the binding of [125I-Tyr1]bradykinin to nervous tissue, were found to be increased in the dorsal medulla and hypophysis, and to be decreased in the pineal gland, of spontaneously hypertensive rats. 5. Therefore, the central kinin system may participate, by both pre- and post-synaptic mechanisms, in the maintenance of hypertension in spontaneously hypertensive rats.

Contribution of Vascular Nitric Oxide to Basal Blood Pressure in Conscious Spontaneously Hypertensive Rats and Normotensive Wistar Kyoto Rats

1995 ◽  
Vol 89 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Naoyoshi Minami ◽  
Yutaka Imai ◽  
Jun-Ichiro Hashimoto ◽  
Keishi Abe
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Basal Blood Pressure ◽  
Wistar Kyoto

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, Nω-l-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20–28 weeks. To estimate the ‘amplifier property’ of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured. 3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 ± 9 mmHg to 67 ± 2 mmHg and from 117 ± 2 mmHg to 49 ± 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of Nω-l-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats. The absolute changes in mean arterial pressure elicited by Nω-l-arginine methyl ester were significantly greater in spontaneously hypertensive than in Wistar Kyoto rats (P < 0.01), but there was no significant difference in the responses to Nω-l-arginine methyl ester when they were expressed as percentages of either the lower blood pressure plateau or maximum blood pressure. 4. These results indicate that basal blood pressure in both spontaneous hypertensive and Wistar Kyoto rats is maintained by a balance between vascular nitric oxide and major pressor systems. They also suggest that the vasodilatory effect of vascular nitric oxide does not differ between spontaneously hypertensive and Wistar Kyoto rats, and that the increased pressor effect of Nω-l-arginine methyl ester in spontaneously hypertensive rats is due to a vascular amplifier mechanism.

Calmodulin levels in hypertensive rats

1985 ◽  
Vol 68 (4) ◽  
pp. 407-410 ◽  
Author(s):  
J. Higaki ◽  
T. Ogihara ◽  
Y. Kumahara ◽  
E. L. Bravo
Keyword(s):  
Intracellular Calcium ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Deoxycorticosterone Acetate ◽  
Spontaneously Hypertensive ◽  
Calcium Dependent ◽  
Wistar Kyoto Rats ◽  
Regulatory Systems ◽  
Wistar Kyoto ◽  
The Brain

1. Intracellular calmodulin levels were measured by direct radioimmunoassay in spontaneously hypertensive rats (SHR) and Wistar—Kyoto rats (WKY). 2. Decreased calmodulin levels were demonstrated in the brain, heart, aorta and kidney of spontaneously hypertensive rats compared with those in Wistar—Kyoto rats. 3. Calmodulin levels in the brain were also decreased in deoxycorticosterone acetate (DOCA)-salt rats, but not changed significantly in the heart, aorta and kidney compared with those in Wistar—Kyoto rats. 4. These findings suggest that intracellular calcium-dependent regulatory systems are genetically disrupted in spontaneously hypertensive rats, but this is probably not an important factor in the development of hypertension.

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