Physiologic Responses to Chronic Dietary Tyrosine Supplementation in DOCA-Salt-Treated Rats

The endocrine (plasma renin activity, insulin and ADH) and hemodynamic responses (heart rate and mean arterial pressure) to isoprenaline infusion were examined in conscious deoxycorticosterone-salt hypertensive rats (DS) and compared with uninephrectomized-salt control rats (US). A dose-related rise in plasma renin activity and plasma insulin values was found in US rats, while no change in either parameter was observed in DS rats after 30 min of isoprenaline infusion. ADH was not increased in US rats at any dose of isoprenaline infusion. However, in DS rats the largest dose (450 ng/kg/min) produced a significant rise. Isoprenaline infusion increased the heart rate in both groups, but the increases in the DS group were significantly lower than in the US group for the 200-ng/kg/ min dose (p < 0.01). The drop in mean arterial pressure was found to be more pronounced in DS rats than in US rats at 50, 100 and 200-ng/kg/min isoprenaline doses. Recovery of the mean arterial pressure to basal levels was also found in US rats with the various doses of isoprenaline administered. However, in DS rats the different doses of isoprenaline produced a progressive drop in mean arterial pressure with no recovery at the end of 30 min of isoprenaline infusion. The present results provide no evidence of subsensitivity to isoprenaline in the resistance vessels of conscious DS rats and suggest that the greater hypotensive response observed in these rats may be due to the inability of the renin-angiotensin system to adequately compensate the vasodilation produced by isoprenaline.

Section: Hemodynamic Studysupporting

confidence: 93%

β-Adrenergic Reactivity in Conscious DOCA-Salt Hypertensive Rats

Vargas

Jm²,

García-Torres³

et al. 1989

“…Volume, epinephrine, norepineph rine and creatinine concentrations were measured. Urinary catecholamines were measured by high-pres sure liquid chromatography with electrochemical de tection as described earlier [4,21]. Urinary creatinine was measured by the method of Chasson et al [6], adapted for the Technicon autoanalyzer.…”

Section: Methodsmentioning

confidence: 99%

Effect of Chronic Treatment with Clonidine and Spironolactone on Cold-Induced Elevation of Blood Pressure

Baron

Riesselmann²,

Fregly³

1991

Self Cite

The present study was designed to determine whether antihypertensive agents known to affect the renin-angiotensin-aldosterone (RAA) system might affect the elevation of blood pressure induced by chronic exposure to cold. Spironolactone, a mineralocorticoid receptor blocker, was added to the food and administered to rats chronically exposed to cold. In addition, clonidine, an α₂-adrenergic agonist and inhibitor of renin secretion, was administered to another group of cold-exposed rats by daily intraperitoneal injection. A warm-adapted and a cold-treated control group were also used. Chronic administration of spironolactone prevented the development of hypertension but failed to prevent other adaptive physiological changes characteristically occurring during exposure to cold and seen in the cold-treated control rats. Thus, increased weight of the heart, kidneys, adrenals and brown adipose tissue, increased dipsogenic responsiveness to angiotensin II, increased urinary outputs of norepinephrine and epinephrine, and increased food and water consumption were observed in all rats, treated and untreated, during exposure to cold. Similarly, daily injection of clonidine attenuated the elevation of blood pressure but also failed to prevent the other adaptive physiological changes characteristic of cold. These results are consistent with the hypothesis that the RAA system plays a role in the development of the cold-induced elevation of blood pressure.

“…The urine collected was analyzed for its concen trations of sodium and potassium (flame photome try), creatinine [4], and catecholamines (norepineph rine, epinephrine, and dopamine) by high-pressure liquid chromatography with electrochemical detec tion [3,13].…”

Section: Experiments 2: Effect O F Chronic Dietarytreatment With L-trymentioning

confidence: 99%

Effect of Chronic Dietary Treatment with L-Tryptophan on the Development of Renal Hypertension in Rats

Fregly¹,

Lockley²,

Cade³

1988

Self Cite

Chronic dietary administration of L-tryptophan (2.5 and 5.0 g/100 g food) to rats provided significant protection against the development of hypertension induced by bilateral encapsulation of the kidneys with latex envelopes. Lower doses of tryptophan (0.5 and 1.0 g/100 g food) attenuated the rate of elevation of blood pressure, but failed to maintain systolic blood pressures at levels significantly below that of untreated renal hypertensive controls. The body weight of the rats was not affected significantly by treatment with any dose of tryptophan used. Chronic treatment with tryptophan also protected against the reduced urinary concentrating ability during a 24-hour dehydration that characteristically accompanies renal encapsulation. A modest (5–8%) effect of treatment to reduce cardiac hypertrophy was also observed. The mechanism of the antihypertensive effect of tryptophan is not revealed by these studies although they rule out the possibilities that reduction in sodium intake and/or reduction in body weight may be important factors.