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Biomedical subjects

R J Contreras

Publications and source records attributed to R J Contreras.

6 recordsLinked to original sources
PubMed1992

Sex difference in blood pressure of spontaneously hypertensive rats influenced by perinatal NaCl exposure.

Our prior study showed that the basal blood pressure level and pressor response to peripheral angiotensin II of adult Sprague-Dawley rats were enhanced by perinatal exposure to a high NaCl diet. The purpose of the present study was to assess further the relationship between NaCl-sensitivity of blood pressure and perinatal NaCl exposure. We tested the hypothesis that the basal blood pressure level and pressor responses to angiotensin II could be increased by perinatal exposure to high NaCl in NaCl-resistant spontaneously hypertensive rats (SHR-R). Adult female SHR-R were maintained on a diet containing either basal 1% or high 8% NaCl throughout pregnancy and lactation. The offspring were continued on these same diets to 30 days postpartum. Thereafter, all offspring were maintained on a diet containing 1% NaCl. After being adapted to restraint, systolic blood pressure was measured indirectly by the tail-cuff procedure when the rats were 30, 44, and 58 days of age. Subsequently, baseline mean arterial pressure (MAP) and pressor responses to intravenous administration of angiotensin II (20, 40, 80, and 120 ng/kg body weight) were obtained from the catheterized femoral artery in conscious unrestrained rats. The MAP levels of adult female SHR-R exposed perinatally to 8% NaCl were significantly greater than those of females exposed to 1% NaCl. This elevated blood pressure was accompanied by an elevation in plasma osmolality. Perinatal exposure to 8% NaCl did not raise the blood pressure and plasma osmolality levels of adult male SHR-R, but did enhance pressor responses to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1991

Dietary obesity and weight cycling in rats: a model of stress-induced hypertension?

The present study was designed to reproduce the mild hypertension seen in dietary obese weight-cycled rats [P. Ernsberger and D. O. Nelson. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R47-R55, 1988] and determine whether this mild hypertension was associated with changes in sodium excretion and pressor responsiveness to angiotensin II (ANG II). Male Sprague-Dawley rats were fed pelleted chow (Pellet group) or chow plus sweetened condensed milk (Milk group) or were exposed to four cycles of a 4-day fast alternated with 2 wk of refeeding of pelleted chow and sweetened condensed milk (Cycled group). Blood pressure and heart rate were measured by tail cuff at the onset and last day of each fast and after 3 days of refeeding. During fasting, urine sodium excretion was measured. Mean arterial pressure and heart rate responses to intravenous administration of ANG II (40, 80, and 120 ng/kg), metoprolol (1 mg/kg), and methyl scopolamine (2 mg/kg) were obtained from the femoral artery in awake unrestrained rats. Weight cycling did not lead to mild hypertension or increased bradycardic response to sympathetic blockade with metoprolol. ANG II-elicited pressor responses were similar for Pellet, Milk, and Cycled groups. Sodium excretion did not change with fasting. Mild hypertension developed when obese weight-cycled rats were housed together in groups and not when housed individually. Our preliminary data are consistent with the notion that stress associated with group housing may be a factor in the mild hypertension of obese weight-cycled rats.

Animals↗
PubMed1990

Dissociation of autonomic controls of heart rate in weaning-aged borderline hypertensive rats by perinatal NaCl.

The ontogeny of functional sympathetic neural, adrenal medullary, and extra-adrenal components of adrenergic control of heart rate was investigated in borderline hypertensive rats exposed to either high or low sodium chloride (NaCl) from conception through weaning. Borderline hypertensive rats were produced by mating spontaneously hypertensive females with normotensive Wistar-Kyoto males. Females were maintained on diets containing either low (0.12% NaCl) or high (3% NaCl) dietary NaCl throughout pregnancy and lactation. At 28 days of age, baseline heart rates recorded from awake and unrestrained pups did not differ between low and high NaCl-exposed pups. Overall sympathetic tone, inferred from heart rate change after beta 1-adrenergic blockade with atenolol, did not differ between high and low NaCl-exposed pups. Early NaCl exposure did not alter the neural component of sympathetic control of heart rate as inferred from heart rate decrease after bretylium tosylate. Parasympathetic nervous system control, as reflected by tachycardic response to muscarinic receptor blockade with atropine methyl nitrate was also unchanged by early NaCl exposure. The adrenal catecholamine component of sympathetic control of heart rate was inferred from bradycardia following administration of the ganglion blocking agent, chlorisondamine, to pups pretreated with bretylium and atropine methyl nitrate. Pups exposed to low NaCl showed increased adrenal control of heart rate compared to high NaCl-exposed pups. The influence of residual catecholamines on heart rate was inferred from bradycardia following administration of the beta 1-adrenergic receptor blocking agent, atenolol, in pups pretreated with bretylium, atropine methyl nitrate, and chlorisondamine. Residual catecholamine influence was greater in rats exposed to high NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗
PubMed1979

Sodium deprivation alters neural responses to gustatory stimuli.

The effects of sodium deprivation for 10 d, a period sufficient to induce sodium appetite, on gustatory nerve discharges in rats were determined. Chorda tympani responses to concentration series of sodium chloride, sucrose, hydrochloric acid, and quinine hydrochloride were recorded and analyzed without the experimenter knowing the animal's deprivation condition. After deprivation, both whole nerve and single nerve fiber responses to sodium chloride were smaller; NaCl-best fibers, those more responsive to sodium chloride than to sucrose, hydrochloric acid, or quinine, were most affected. Thresholds had not changed; however, slopes of the stimulus-response functions for sodium chloride were lowered. Comparable changes in responses to the other stimuli did not occur. These results were discussed with respect to a possible relationship between changes in sodium chloride responsivity and changes in sodium intake, differences between methods of inducing sodium appetite, coding of taste quality and intensity, and mechanisms which might effect the responsivity change.

Animals↗
PubMed1978

Salt taste and disease.

Sodium appetite reflects the importance of sodium homeostasis and the relative scarcity of sodium for many terrestrial animals. Man, for various reasons, also seems to have a specific preference for salt which he consumes in excess of need, and this has been characterized as an important contributor to hypertension. Gustatory sensibility is necessary for the development of sodium appetite. Thus, research on the possible role salt taste sensitivity plays in controlling NaCl consumption in the sodium deficient rat was reviewed as a potential model for the study of salt taste and hypertension in man. Taste acuity experiments began first by examining salt taste thresholds. These studies found that thresholds were not altered by sodium deficiency in rat and the results in hypertensive humans were inconclusive. Threshold determinations may not reveal true sensitivity differences because they varied significantly across experiments and because they are restricted to a small portion of the intensity domain. When research was directed to suprathreshold stimuli, concentrations a rat or man might normally experience, the evidence suggested that hypertensive humans, like sodium-deficient rats, were less sensitive to the taste of salt. This reduced sensitivity may account, in part, for the fact that these two groups consume more salt.

Adrenal Glands↗