Interaction between the renin-angiotensin and beta adrenergic nervous systems in drinking and pressor responses after renal artery constriction.

Constriction of the remaining renal artery of a uninephrectomized rat produced an increase in plasma renin level, a decrease in renal cortex renin level, an increase in blood pressure and a drinking response. Simultaneous infusion with the angiotensin II antagonist, saralasin, potentiated the rise in plasma renin level and blocked the rise in blood pressure. Drinking was only partially attenuated. Pretreatment with l-propranolol had no effect on the changes in plasma or kidney renin levels, but the increase in blood pressure was potentiated and the drinking response was attenuated. It is concluded that the pressor and drinking responses to renal artery constriction are partially mediated by the beta adrenergic nervous system.

Effect of chronic clonidine treatment and its abrupt cessation on mean blood pressure of rats with a normal or an elevated blood pressure.

1. Clonidine (6 mg of base/l of water) was given as drinking fluid to normotensive rats or rats with established or early hypertension. 2. Spontaneous hypertensive rats (6 months old: average dose of clonidine, 0.6 mg 24 h-1 kg-1) showed a sustained fall in blood pressure over 3 weeks. 3. The same clonidine solution given for 6 weeks to two-kidney Goldblatt rats with early-stage hypertension (average dose of clonidine: 1 mg 24 h-1 kg-1) or spontaneously hypertensive rats (clonidine dose: 1 mg) induced a fall in mean blood pressure, but no change in normotensive rats. 4. Replacement of clonidine by water induced hypertension and lability which led to death in hypertensive but not in normotensive rats.

Lithium concentrations in saliva, plasma and red blood cells of patients given lithium acetate.

Lithium concentrations in saliva, plasma and red blood cells were measured in: 1) six hospitalized patients under long-term lithium therapy, at 2, 5, 9 and 24 hours after oral doses of 24 mEq Li acetate and 2 or 12 hours after 8 mEq Li acetate; and 2) 10 outpatients under chronic lithium treatment at two occasions 8 days apart. With changing plasma concentrations, [Li] saliva varied without any notable time lag. [Li] saliva was always much higher than [Li] plasma. The ratio [Li] saliva/ [Li] plasma water averaged 3.2 +/- 0.2 in 62 determinations, but varied widely at different times after oral lithium in the same individuals and less widely between different individuals. "Prediction" of plasma lithium concentration from measured [Li] saliva appears hazardous, and may provide reliable indications only if [Li] saliva is measured repeatedly. Salivary lithium concentrations were not correlated with either potassium or sodium concentrations. Lithium concentrations in red blood cells were always lower than in plasma: [Li] red blood cell water/ [Li] plasma water averaged 0.37 +/- 0.03. With changing plasma concentrations, rise and fall of red blood cell lithium lagged considerably behind plasma changes. This resulted in a rise of the red blood cell/plasma concentration ratio from a very low value 2 hours after an oral dose to a rather high value 24 hours after an oral dose.