1. The acute malignant phase of hypertension in rats with an untouched contralateral kidney is characterized by salt and fluid loss, increased fluid intake, decrease in body-weight gain, and reduced food consumption. Plasma concentrations of sodium and potassium were reduced, and plasma angiotensin II rose to about four times normal. 2. To investigate the significance of an untouched contralateral kidney for the development of the acute malignant phase in renal hypertensive rats, comparative studies were undertaken in unilaterally nephrectomized rats with stenosis of the remaining renal artery and in rats with bilateral renal artery stenosis. In addition, the effect of declamping one renal artery in rats with bilateral stenosis was studied. 3. In unilaterally nephrectomized rats, no signs of sodium and fluid loss were demonstrable, despite marked increase in blood pressure. Similarly, rats with bilateral renal artery stenosis had no acute malignant phase of hypertension. 4. In hypertensive rats with bilateral stenosis, removal of the clip from one renal artery was followed by an immediate fall in blood pressure and a subsequent gradual increase. Eleven of sixteen rats lost salt and fluid and developed an acute malignant phase. Plasma angiotensin II was high and serum urea elevated. 5. Consumption of 2% saline in addition to water as drinking fluid had a beneficial effect, since only five of fourteen rats showed signs of the acute malignant phase, which were milder than in rats on water only. 6. It is concluded that the untouched contralateral kidney is responsible for the negative salt and water balance and its consequences, which are characteristic of the acute malignant phase of experimental renal hypertension.

Animals↗

PubMedDate not supplied

Regulation of renin release and intrarenal formation of angiotensin. Studies in the isolated perfused rat kidney.

1. Isolated rat kidneys were perfused at a constant pressure of 90 mmHg in a single-pass system with either a cell-free medium or a suspension of washed bovine red blood cells, free of the components of the renin-angiotensin system. In red blood cell perfused kidneys renal haemodynamics and sodium reabsorption corresponded closer to values observed in the intact rat than in cell-free perfused kidneys. 2. In red blood cell-perfused kidneys in the absence of plasma renin substrate autoregulation of renal blood flow was almost complete at pressures above 90 mmHg, provided that perfusion pressure was changed rapidly. 3. Renin release varied inversely with perfusion pressure within a pressure range from 50 to 150 mmHg; the greatest changes of renin release occurred, when perfusion pressure was reduced from 90 to 70 mmHg; maximal stimulation of renin release was observed at 50 mmHg. After reduction of perfusion pressure, renin release immediately started to rise and reached a new level within 5 min. Local reduction of perfusion pressure in small arteries and arterioles by the injection of microspheres induced a short-lasting decrease in renal plasma flow and a transient stimulation of renin release. 4. High concentrations of furosemide stimulated renin release by a direct intrarenal mechanism. 5. Isoproterenol stimulated renin release in low concentrations without a concomitant vasodilation, whereas high concentrations induced an increase in both renal plasma flow and renin release. The effects of isoproterenol were completely blocked by propranolol. 6. Sodium nitroprusside induced similar increases in renal plasma flow, as did high concentrations of isoproterenol, but only a small and slow increase in renin release was observed. 7. Angiotensin II (AII) suppressed renin release in concentrations corresponding to plasma levels measured in the intact rat independently of its vasoconstrictor effects, whereas vasopressin in antidiuretic concentrations did not affect renin release. 8. AII, AI, synthetic tetradecapeptide renin substrate (TDP), crude and purified rat plasma renin substrate induced a dose-dependent reduction in renal plasma flow. SQ 20 881, a competitive inhibitor of converting enzyme, and low doses of 1-Sar-8-Ala-AII (saralasin), a competitive antagonist of AII, did not change renal plasma flow, whereas high concentrations of saralasin had a vasoconstrictor effect on their own. 9. Saralasin inhibited the vasoconstrictor effects of AII and TDP to a similar degree. SQ 20 881 inhibited the vasoconstrictor effects of AI and purified renin substrate, but did not influence the actions of TDP and the crude renin substrate preparation. 10. From these data it is concluded, that AI is converted into AII within the kidney at a rate of 1-2%. The vasoconstriction induced by the crude renin substrate probably does not involve the AII receptors. TDP may act by itself on the AII receptors or via the direct intrarenal formation of AII...

Angiotensin II↗

PubMedDate not supplied

Fluid and salt intake during the development of renal hypertension in rats.

1. In Sprague-Dawley rats, two-kidney, one-clip renal hypertension was induced, and the drinking behaviour as well as total fluid and sodium intake were studied before and for 16 days after the operation. 2. When water alone was offered as drinking fluid, the blood pressure reached values that were by about 20 mmHg higher than those in the rats which had free choice of drinking water or 2% saline. 3. In those rats which had water and 2% saline to drink, the total sodium and fluid intake rose transiently for three days, as compared with that of the sham-operated controls, and increased steeply starting from the 7th and 10th day, respectively. When a tighter stenosis of the renal artery was induced, the pressure rose more rapidly, and the total fluid and sodium intake increased continuously after the operation until the end of the experiment. 4. A positive correlation was demonstrable between the height of blood pressure and the total daily intake of fluid and sodium, respectively. 5. The relation between the total daily fluid and the total daily sodium intake followed a straight regression line. 6. The hypertensive rats which had a high total sodium intake responded to the withdrawal of the 2% saline solution, within 2 days, with increased water intake, decreased food intake, and loss of body weight, whereas the blood pressure remained high. 7. In the two-kidney, one-clip hypertension, no 'critical level of blood pressure' can be defined, beyond which the contralateral kidney starts to lose sodium.

Animals↗

PubMedDate not supplied

Effects of neonatal sympathectomy by 6-hydroxydopamine on blood pressure and intravascular volume in young stroke-prone spontaneously hypertensive rats.

1. Stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY) were 'chemically sympathectomized' immediately after birth with 6-hydroxydopamine (6-OHDA, 100 mg/kg s.c. daily) for the first 10 days of life. 2. Body weight gain was diminished in both groups as compared with sham-treated controls. Blood pressure was reduced in 'sympathectomized' SHRSP, and also WKY rats had a slightly lower blood pressure than control rats. 3. Plasma concentration of angiotensin II and renin content of the kidney were not influenced by 6-OHDA. 4. 'Sympathectomized' SHRSP retained similar amounts of sodium than sham-treated SHRSP when sodium retention is expressed per body weight gained. Plasma and blood volumes were increased in both SHRSP and WKY rats, whereas packed cell volume was significantly decreased. 5. These results demonstrate the significance of an intact sympathetic nervous system for the development of hypertension in SHRSP. The expanded plasma and blood volume in 'sympathectomized' rats indicate an important role of the sympathetic nervous system and/or the arterial blood pressure for the regulation of intravascular volume.

Angiotensin II↗

PubMedDate not supplied

Vasopressin and vascular reactivity in the development of DOCA hypertension in rats with hereditary diabetes insipidus.

To examine the role of vasopressin (VP) in DOCA-salt hypertension, arterial pressure and renal vascular reactivity were studied in control Long-Evans (LE) rats and in Brattleboro rats homozygous for diabetes insipidus (DI rats). Vascular reactivity to norepinephrine, VP and angiotensin II was assessed in isolated kidneys perfused at constant flow. LE rats showed an increase in arterial pressure (AP) which was significant at 2 weeks post DOCA and averaged 180 mm Hg at 4 weeks. DI rats lacking VP showed no rise in AP after DOCA; however, DI rats given VP and DOCA developed hypertension with a course and magnitude similar to that observed in LE rats. At 6 to 10 weeks post DOCA, renal vascular reactivity to all agents was increased in LE rats and DI rats replaced with VP. Normotensive DI rats lacking VP showed depressed reactivity. Assessment of changes in reactivity at 3 days post DOCA showed that changes preceded the rise in AP. These data suggest that VP may play a primary role in the pathogenesis of DOCA hypertension and that its mechanism may involve an induction of increased vascular reactivity.

Animals↗

PubMedDate not supplied

Strange companionship.

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Blood Pressure↗

PubMedDate not supplied

Practical problems in hypertension management. Introductory remarks.

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Blood Pressure↗

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[Phototherapy in psychiatry: clinical update and review of indications].

Phototherapy introduced in 1984 by Rosenthal as a treatment for SAD (Seasonal Affective Disorder) is the first therapeutic answer to season-related psychopathology. Findings in chronobiology have largely contributed to pathophysiological theories of disorders in the internal circadian system. Actual researches on the etiology of SAD covers fields as retinal deficiency (i.e. disorder of photoreceptors), phase disturbance of the internal circadian rhythms given by internal oscillators and neuroendocrinologically drived disorders, supposing that melatonin is the main mediator of human circadian systems in the CNS. Disorders of the neurotransmitters are an other explored cue. Recent longitudinal studies show a prevalence of seasonal depressive symptoms in general population up to 10%. In populations treated for depression the prevalence of SAD is up to 20%. The SAD sex-ratio (women/men) of 3/1 is found repeatedly. Above 55 years SAD get rare. Effectiveness of phototherapy is showed in nearly all controlled studies. Bright light for patients with mild SAD appears to be most effective as is also the authors clinical impression through the practice of phototherapy in Geneva since 1991. A true placebo for bright light is still to be found according to enable evaluation of potentially important impact that unspecific therapeutic factors may trigger in phototherapy. Actually possible new indications for phototherapy are being explored: bright light for non seasonal depression has been tested with features with SAD; effectiveness in bulimia has been suggested and recently sleep disorders in psychogeriatric patients have been improved. Non seasonal circadian disorders such as jet lag might be sensitive to light.

Adult↗