Effect of green tea rich in gamma-aminobutyric acid on blood pressure of Dahl salt-sensitive rats.

gamma-Aminobutyric acid (GABA) is known to be involved in the regulation of blood pressure by modulating the neurotransmitter release in the central and peripheral sympathetic nervous systems. This study investigated the antihypertensive effect of green tea rich in GABA (GABA-rich tea) in young and old Dahl salt-sensitive (S) rats. GABA-rich tea was made by fermenting fresh green tea leaves under nitrogen gas. In experiment 1, 21 11-month-old rats, fed a 4% NaCl diet for 3 weeks, were given water (group W), an ordinary tea solution (group T), or a GABA-rich tea solution (group G) for 4 weeks. The average GABA intake was 4.0 mg/rat per day. After 4 weeks of the treatment, blood pressure was significantly decreased in group G (176 +/- 4; P < .01) compared with group W (207 +/- 9) or group T (193 +/- 5 mm Hg). Plasma GABA levels were more elevated in group G (111 +/- 54) than in group W (not detectable) or group T (14 +/- 8 ng/mL; P < .01 v G). In experiment 2, 21 5-week-old rats, fed a 4% NaCl diet, were divided into groups W, T, and G. The average GABA intake was 1.8 mg/rat per day. Body weight or chow and beverage consumption did not differ significantly among the three groups. After 4 weeks of the treatment, although blood pressure was comparable in groups W and T (165 +/- 3 v 164 +/- 5 mm Hg, mean +/- SE), it was significantly lower in group G (142 +/- 3 mm Hg) than in the other groups (P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Reduction of blood pressure in salt-fed Dahl salt-sensitive rats with diets rich in olive oil, safflower oil or calcium biphosphate but not with calcium carbonate.

Increased dietary calcium as CaCO3 had no effect in NaCl-induced hypertension in Dahl salt-sensitive (Dahl-S) rats, while the calcium supplementation as CaHPO4 did lower the blood pressure (BP). A diet rich in either monounsaturated or polyunsaturated fatty acids produced a significant lowering of blood pressure compared with the relatively saturated palm-oil diet in NaCl-induced hypertension in Dahl-S rats. The lower BP found with olive oil is probably not related to increased amounts of PGE2 and PGI2.

Potassium reduces cerebral hemorrhage and death rate in hypertensive rats, even when blood pressure is not lowered.

In a study of the effects of K+ in stroke prone spontaneously hypertensive rats, adding K+ to normal chow was found to reduce the mortality from 83% to 2%, a 98% reduction. An 86% reduction in mortality occurred even when blood pressure was virtually equal in the two stroke prone spontaneously hypertensive groups being compared. Dietary K+ supplements also reduced mortality in hypertensive Dahl salt-sensitive rats from 55% to 4%, a 93% reduction. There was an 87% reduction in mortality even when blood pressure was equal in the Dahl salt-sensitive groups being compared. The added dietary K+ decreased blood pressure moderately in stroke prone spontaneously hypertensive rats and modestly in Dahl salt-sensitive rats, which probably contributed to the reduced death rate. More importantly, however, the added K+ seemed to prevent severe lesions in cerebral arteries and deaths even when blood pressure lowering was eliminated as a protective factor. In another group of stroke prone spontaneously hypertensive rats, there was a 40% incidence of cerebral hemorrhage in surviving rats not receiving K+ supplements and no incidence of cerebral hemorrhage in similar surviving rats receiving K+ supplements, which suggests that K+ supplements confer protection against brain hemorrhage.

Potassium prevents death from strokes in hypertensive rats without lowering blood pressure.

Adding potassium to normal chow reduces death rate in hypertensive stroke-prone (SHRSP) rats from 83 to 2%, a 98% reduction. An 86% reduction in deaths occurred even when blood pressure (BP) was virtually equal in the two SHRSP groups being compared. Potassium supplements in the diet also reduced stroke deaths in hypertensive Dahl S rats from 55 to 4%, a 93% reduction. There was an 87% reduction in deaths even when BP was actually equal in the two Dahl S groups being compared. The added potassium in the diets decreased BP moderately in SHRSP rats and modestly in Dahl S rats, which contributed somewhat to the reduction in strokes. However, more importantly, the added potassium seems to reduce the intrinsic susceptibility to cerebral artery lesions for a given level of hypertension, even when BP is not lowered.

Prevention of malignant hypertension in salt loaded "S" Dahl rats with the calcium antagonist nifedipine.

Female "S" Dahl rats, fed an 8% NaCl diet from the 6th week of age developed malignant hypertension and heart hypertrophy in the course of 6 weeks on the salt regimen. Simultaneous treatment with nifedipine (300 ppm in diet additional to 8% NaCl) prevented the increase in blood pressure, reduced heart hypertrophy and mortality and improved the impaired renal function in "S" rats. The decrease in hematocrit in salt loaded "S" rats was prevented by nifedipine. The prophylactic effect of the calcium antagonist nifedipine is only partly due to the prevention of increase in systemic vascular resistance. In addition an improvement of failed intrarenal hemodynamics by nifedipine can be postulated. This enables the kidney of "S" rats to excrete the salt load without increasing blood pressure and plasma volume.

Paraventricular--suprachiasmatic lesions prevent salt-induced hypertension in Dahl rats.

1. We studied the effects that lesions produced in the paraventricular and suprachiasmatic nuclei and intervening periventricular area had on 24 h mean circadian blood pressures in Dahl salt-sensitive and -resistant rats and their sham-operated controls. We measured blood pressures while the animals were on a low salt diet and after 1, 5 and 13 weeks of 8% NaCl diet. 2. Salt-sensitive rats with lesions had lower blood pressures than salt-sensitive sham-operated controls at all points of the study. In contrast, identical lesions in salt-resistant rats produced a transient pressor response to the diet. Twenty-four hour mean heart rate, determined after 13 weeks of 8% NaCl intake, was low only in salt-sensitive rats with lesions. Sodium intake and excretion per kg of body weight, as well as plasma sodium concentrations, were similar in all groups. 3. We conclude that the anteromedial hypothalamic area, which includes the paraventricular nucleus, the suprachiasmatic nucleus and the intervening periventricular area, participates in the development of Dahl hypertension. We suggest that a multifactorial mechanism is involved: (a) the facilitatory role of this region in ACTH release, (b) this region's participation in the baroreceptor reflex via vasopressinergic efferents to the nucleus of the tractus solitarius, and (c) the roles of the paraventricular and suprachiasmatic nuclei in the regulation of salt and water balance.

Brain lesions in the paraventricular nuclei and catecholaminergic neurons minimize salt hypertension in Dahl salt-sensitive rats.

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 blood 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.

Genetic influence on brain catecholamines: high brain noradrenaline in salt-sensitive rats.

1. Rats genetically sensitive to salt-induced hypertension showed higher levels of plasma noradrenaline and adrenaline than rats genetically resistant to hypertension. 2. The hypertension-sensitive rats had higher hypothalamic noradrenaline and lower adrenaline than resistant rats. 3. In response to a high salt diet brain-stem noradrenaline increased in sensitive rats and resistant rats exhibited a decrease on the same diet.