Brain Lesions in the Paraventricular Nuclei and Catecholaminergic Neurons Minimize Salt Hypertension in Dahl Salt-Sensitive Rats

1981 ◽  
Vol 61 (s7) ◽  
pp. 53s-55s ◽  
Author(s):  
Atsuo Goto ◽  
Toshio Ikeda ◽  
Louis Tobian ◽  
Junichi Iwai ◽  
Mary A. Johnson
Keyword(s):  
Blood Pressure ◽  
Brain Lesions ◽  
Suprachiasmatic Nuclei ◽  
Catecholaminergic Neurons ◽  
Paraventricular Nuclei ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Electrolytic Lesions ◽  
The Central Nervous System ◽  
6 Hydroxydopamine

1. The rise in blood pressure in Dahl salt-sensitive rats that received intracerebroventricular 6-hydroxydopamine was almost half that of the control rats throughout 20 weeks of high (8%) NaCl feeding. 2. The rise in bood pressure in Dahl salt-sensitive rats with bilateral complete electrolytic lesions of the paraventricular nuclei was almost half that of the control rats during 12 weeks of high (8%) NaCl feeding. 3. The bilateral complete electrolytic lesions of the suprachiasmatic nuclei enhanced the development of NaCl hypertension in Dahl salt-sensitive rats. 4. These results show that NaCl-induced hypertension in Dahl salt-sensitive rats requires the integrity of the central nervous system catecholaminergic neurones and the paraventricular nuclei for its full expression.

Central catecholamine depletion, vasopressin, and blood pressure in the DOCA/NaCl rat

1983 ◽  
Vol 244 (6) ◽  
pp. H807-H813 ◽  
Author(s):  
T. Okuno ◽  
S. R. Winternitz ◽  
M. D. Lindheimer ◽  
S. Oparil
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Chemical Sympathectomy ◽  
Sprague Dawley ◽  
Paraventricular Nuclei ◽  
Sprague Dawley Rats ◽  
Intraventricular Injections ◽  
The Central Nervous System ◽  
6 Hydroxydopamine

To determine whether impaired arginine vasopressin (AVP) release occurs when DOCA-NaCl hypertension is prevented following chemical sympathectomy with 6-hydroxydopamine (6-OHDA), male Sprague-Dawley rats treated with intraventricular injections of 6-OHDA (250 micrograms X 2) or Merlis solution received deoxycorticosterone acetate (DOCA) implants (100 mg/kg) and drank 0.5% saline. Systolic blood pressure in the 6-OHDA-treated DOCA/NaCl group (139 +/- 4 mmHg) was lower (P less than 0.001) than in the Merlis-DOCA/NaCl group (183 +/- 7 mmHg). 6-OHDA treatment produced widespread catecholamine depletion throughout the central nervous system, including the supraoptic and paraventricular nuclei, the cells of which are known to produce AVP, but hypothalamic, pituitary, and plasma AVP levels were similar in both experimental groups, the latter values averaging 1.5–2 times those of controls. Both groups of rats suppressed AVP secretion appropriately when water loaded. Such suppression, however, had no effect on blood pressure in the hypertensive animals and, furthermore, administration of the AVP antagonist d(CH2)5Tyr(Me)AVP produced small decrements in mean blood pressure of both groups that were not significantly different from responses seen in control normotensive rats. These data demonstrate that 6-OHDA does not prevent DOCA-NaCl hypertension by decreasing AVP levels and suggest that AVP is not necessary for the maintenance of hypertension in this model.

PVN lesions prevent the endothelin 1-induced increase in arterial pressure and vasopressin

2001 ◽  
Vol 280 (2) ◽  
pp. E349-E356 ◽  
Author(s):  
Noreen F. Rossi ◽  
Haiping Chen
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Arterial Pressure ◽  
Paraventricular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Electrolytic Lesions ◽  
The Central Nervous System ◽  
Baseline Values ◽  
Long Evans

Endothelin (ET) acts within the central nervous system to increase arterial pressure and arginine vasopressin (AVP) secretion. This study assessed the role of the paraventricular nuclei (PVN) in these actions. Intracerebroventricular ET-1 (10 pmol) or the ETA antagonist BQ-123 (40 nmol) was administered in conscious intact or sinoaortic-denervated (SAD) Long-Evans rats with sham or bilateral electrolytic lesions of the magnocellular region of the PVN. Baseline values did not differ among groups, and artificial cerebrospinal fluid (CSF) induced no significant changes. In sham-lesioned rats, ET-1 increased mean arterial pressure (MAP) 15.9 ± 1.3 mmHg in intact and 22.3 ± 2.7 mmHg in SAD ( P < 0.001 ET-1 vs. CSF) rats. PVN lesions abolished the rise in MAP: −0.1 ± 2.8 mmHg in intact and 0.0 ± 2.9 mmHg in SAD. AVP increased in only in the sham-lesioned SAD group 8.6 ± 3.5 pg/ml ( P < 0.001 ET-1 vs. CSF). BQ-123 blocked the responses. Thus the integrity of the PVN is required for intracerebroventricularly administered ET-1 to exert pressor and AVP secretory effects.

Intracerebroventricular infusion of RU28318 blocks aldosterone-salt hypertension

1990 ◽  
Vol 258 (3) ◽  
pp. E482-E484 ◽  
Author(s):  
E. P. Gomez-Sanchez ◽  
C. M. Fort ◽  
C. E. Gomez-Sanchez
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Systolic Blood Pressure ◽  
Urine Volume ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Salt Hypertension ◽  
The Central Nervous System ◽  
Dose Dependent

The chronic intracerebroventricular (icv) infusion of aldosterone in rats and dogs elevates the blood pressure within 10-14 days at doses far below those that produce hypertension systemically. The effect in rats is dose dependent and blocked by the concomitant icv infusion of the antimineralocorticoid, prorenone. The effect of the icv infusion of RU28318, another specific spironolactone mineralocorticoid antagonist, on the hypertension produced by chronic subcutaneous (sc) administration of aldosterone in sensitized rats was reported. Miniosmotic pumps were used to deliver 1 micrograms/h aldosterone sc and 1.1 micrograms/h RU8318 icv. Over a 24-day period the indirect systolic blood pressure of the control, RU28318 icv, and aldosterone sc plus RU28318 icv groups increased from 105 to 123 mmHg and were not significantly different from each other, whereas the aldosterone sc group increased to 156 mmHg. RU28318, icv or sc, did not alter the increase in urine volume produced by aldosterone sc, and there was no significant differences in weight between the groups. This study provides evidence of the importance of the central nervous system in the pathogenesis of hypertension produced by systemic mineralocorticoid excess.

scholarly journals INFLUENCE OF DIETARY POTASSIUM AND SODIUM/POTASSIUM MOLAR RATIOS ON THE DEVELOPMENT OF SALT HYPERTENSION

1972 ◽  
Vol 136 (2) ◽  
pp. 318-330 ◽  
Author(s):  
Lewis K. Dahl ◽  
George Leitl ◽  
Martha Heine
Keyword(s):  
Blood Pressure ◽  
Dietary Sodium ◽  
Molar Ratio ◽  
Molar Ratios ◽  
Dietary Potassium ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Blood Pressures ◽  
Absolute Concentrations ◽  
Dietary Sodium Chloride

Among genetically hypertension-prone rats, dietary sodium (chloride) was demonstrably hypertensinogenic and potassium (chloride) antihypertensinogenic. On diets containing the same NaCl but different KCl concentrations, mean blood pressure was greater in rats receiving less dietary potassium, i.e., diets with a higher Na/K molar ratio. On diets with different absolute concentrations of NaCl and KCl, but the same Na/K molar ratios, rats on the higher absolute NaCl intakes had the higher blood pressures. On diets with different absolute concentrations of NaCl and KCl, and different Na/K molar ratios, a group on a lower absolute NaCl intake but with a higher Na/K ratio could have more hypertension than a group on a higher absolute NaCl intake but with a lower Na/K ratio. At equivalent molar ratios, the respective effects of these two ions on blood pressure were dominated by that of sodium. It was concluded that the dietary Na/K molar ratio can be an important determinant for the severity, or even development, of salt-induced hypertension. The mechanism of the moderating effect of potassium on sodium-induced hypertension was unclear.

Pressor and sympathetic responses to dorsal raphe nucleus infusions of TRH in rats

1990 ◽  
Vol 258 (6) ◽  
pp. R1464-R1471 ◽  
Author(s):  
J. Mattila ◽  
R. D. Bunag
Keyword(s):  
Dorsal Raphe Nucleus ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Serotonergic Neurons ◽  
Catecholaminergic Neurons ◽  
Pressor Responses ◽  
Electrolytic Lesions ◽  
6 Hydroxydopamine ◽  
The Brain ◽  
Dorsal Raphé

Pressor, tachycardic, and sympathoexcitatory responses to intracerebroventricularly (icv) infused thyrotropin-releasing hormone (TRH) were recorded in urethan-anesthetized rats to identify where centrally administered TRH acts in the brain. None of these responses was altered either by electrolytic lesions in the medial preoptic, posterior, or paraventricular hypothalamus or by chemical lesions produced by destroying catecholaminergic neurons with icv infused 6-hydroxydopamine. By contrast, when serotonergic neurons were similarly destroyed with 5,7-dihydroxytryptamine, TRH-induced tachycardia was inhibited. Attendant pressor responses were also inhibited by electrolytic lesions of the dorsal, but not of the median, raphe nucleus. Pressor and sympathoexcitatory responses elicited by infusing TRH directly into the dorsal raphe nucleus resembled those produced by icv infusion, and their magnitude diminished after pentolinium-induced ganglioplegia. These results are compatible with the interpretation that icv infused TRH may produce its cardiovascular and sympathetic effects by acting, at least in part, on serotonergic mechanisms located in the dorsal raphe nucleus.

scholarly journals Mycophenolate Improves Brain–Gut Axis Inducing Remodeling of Gut Microbiota in DOCA-Salt Hypertensive Rats

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1199
Author(s):  
Iñaki Robles-Vera ◽  
Néstor de la Visitación ◽  
Manuel Sánchez ◽  
Manuel Gómez-Guzmán ◽  
Rosario Jiménez ◽  
...  
Keyword(s):  
Anaerobic Bacteria ◽  
Immunosuppressive Drug ◽  
Hypertensive Rats ◽  
Gut Dysbiosis ◽  
Paraventricular Nuclei ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Male Wistar Rats ◽  
Host Blood ◽  
First Time

Microbiota is involved in the host blood pressure (BP) regulation. The immunosuppressive drug mofetil mycophenolate (MMF) ameliorates hypertension. The present study analyzed whether MMF improves dysbiosis in mineralocorticoid-induced hypertension. Male Wistar rats were assigned to three groups: untreated (CTR), deoxycorticosterone acetate (DOCA)-salt, and DOCA treated with MMF for 4 weeks. MMF treatment reduced systolic BP, improved endothelial dysfunction, and reduced oxidative stress and inflammation in aorta. A clear separation in the gut bacterial community between CTR and DOCA groups was found, whereas the cluster belonging to DOCA-MMF group was found to be intermixed. No changes were found at the phylum level among all experimental groups. MMF restored the elevation in lactate-producing bacteria found in DOCA-salt joined to an increase in the acetate-producing bacteria. MMF restored the percentage of anaerobic bacteria in the DOCA-salt group to values similar to control rats. The improvement of gut dysbiosis was associated with an enhanced colonic integrity and a decreased sympathetic drive in the gut. MMF inhibited neuroinflammation in the paraventricular nuclei in the hypothalamus. This study demonstrates for the first time that MMF reduces gut dysbiosis in DOCA-salt hypertension models. This effect seems to be related to its capacity to improve gut integrity due to reduced sympathetic drive in the gut associated with reduced brain neuroinflammation.

scholarly journals Alterations of NO synthase isoforms in brain and kidney of rats with genetic and salt hypertension

2010 ◽  
pp. 997-1009 ◽  
Author(s):  
S Hojná ◽  
J Kuneš ◽  
J Zicha
Keyword(s):  
Blood Pressure ◽  
Pressure Control ◽  
Brain Regions ◽  
No Synthase ◽  
Inos Expression ◽  
Sympathetic Tone ◽  
No Production ◽  
Adult Rats ◽  
Induced Hypertension ◽  
Salt Hypertension

Both brain and peripheral nitric oxide (NO) play a role in the control of blood pressure and circulatory homeostasis. Central NO production seems to counteract angiotensin II-induced enhancement of sympathetic tone. The aim of our study was to evaluate NO synthase (NOS) activity and protein expression of its three isoforms – neuronal (nNOS), endothelial NOS (eNOS) and inducible (iNOS) – in two brain regions involved in blood pressure control (diencephalon and brainstem) as well as in the kidney of young adult rats with either genetic (12-week-old SHR) or saltinduced hypertension (8-week-old Dahl rats). We have demonstrated reduced nNOS and iNOS expression in brainstem of both hypertensive models. In SHR this abnormality was accompanied by attenuated NOS activity and was corrected by chronic captopril treatment which prevented the development of genetic hypertension. In salt hypertensive Dahl rats nNOS and iNOS expression was also decreased in the diencephalon where neural structures important for salt hypertension development are located. As far as peripheral NOS activity and expression is concerned, renal eNOS expression was considerably reduced in both genetic and salt-induced hypertension. In conclusions, we disclosed similar changes of NO system in the brainstem (but not in the diencephalon) of rats with genetic and salt-induced hypertension. Decreased nNOS expression was associated with increased blood pressure due to enhanced sympathetic tone.

HYPOTHALAMIC SEXUAL PRECOCITY IN FEMALE RATS OPERATED SHORTLY AFTER BIRTH

1962 ◽  
Vol 41 (2) ◽  
pp. 301-313 ◽  
Author(s):  
S. Horowitz ◽  
J. J. Van der Werff ten Bosch
Keyword(s):  
Anterior Commissure ◽  
Anterior Hypothalamus ◽  
Female Rats ◽  
Vaginal Opening ◽  
Sexual Precocity ◽  
Paraventricular Nuclei ◽  
Gonadotrophin Secretion ◽  
Electrolytic Lesions

ABSTRACT Electrolytic lesions were placed in the anterior hypothalamus of 3–4 day-old female rats; vaginal opening was hastened in comparison with blank-operated littermates in 12 of 17 rats bearing a lesion in the basal supra-and post-chiasmatic area. In the animals with the earliest vaginal opening, lesions reached upward towards the region of the anterior commissure and the paraventricular nuclei. The degree of advancement of puberty in rats operated at the age of 3 or 4 days was similar to that caused by lesions made at 10, 14 or 15 days. This finding suggests that the effect of a lesion upon gonadotrophin secretion does not begin to take place until after the age of at least two weeks.

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