PRESSER MECHANISMS IN ADRIAMYCIN-INDUCED NEPHROPATHY WITH HYPERTENSION IN RATS

We explored the role of angiotensin II and vasopressin in the maintenance of blood pressure during the nephrotic syndrome of adriamycin-induced nephropathy in rats. All 91 rats treated with adriamycin developed chronic renal failure with nephrotic syndrome, which was more pronounced in the normotensive rats than the 35% who became hypertensive. Angiotensin II blockade with DuP 753 produced a significantly greater hypotensive response in both the adriamycin-hypertensive (-16+/-3 mmHg) and adriamycin-normotensive (-14+/-5 mmHg) groups than the saline-treated controls (-5+/-1 mm Hg, P<.05). Vasopressin blockade with either a V1V2 inhibitor or a selective V-1 inhibitor produced a hypotensive response in adriamycin-hypertensive rats only (by -16+/-4 and -17+/-2 mm Hg, respectively, P<.01), although the nonselective vasopressin inhibitor produced similar fluid loss and body weight reduction in all three groups. The data suggest that in adriamycin-induced nephropathy with nephrotic syndrome, angiotensin II contributes to blood pressure maintenance in both hypertensive and normotensive animals, whereas the presser action of vasopressin contributes to elevated blood pressure in hypertensive animals only.

LEFT-VENTRICULAR MASS ESTIMATED BY M-MODE ECHOCARDIOGRAM IS NOT ALTERED BY CHANGES IN CARDIAC SHAPE AND DIMENSIONS DUE TO ACUTE ARTERIAL-HYPERTENSION

The effect of changes in left ventricular (LV) shape and dimensions due to acute arterial hypertension induced by mechanical obstruction of the aorta for 10 min on LV mass values estimated by M-mode echocardiogram was studied in 14 anesthetized dogs. Although the systolic pressure increased from 117.5 +/- 19.9 to 175.4 +/- 22.9 mmHg altered ventricular diameter from 2.77 +/- 0.49 cm to 3.17 +/- 0.67 cm (P<0.05) and wall thickness from 0.83 +/- 0.09 to 0.75 +/- 0.09 cm (P<0.05), LV mass estimated before (73.5 +/- 19.1 g) and after (78.3 +/- 26.4 g) hypertension was not significantly different. We demonstrate here for the first time that changes in LV dimensions induced by acute arterial hypertension do not modify LV mass values estimated by the M-mode electrocardiogram method.

CHARACTERISTICS OF ARTERIAL-HYPERTENSION IN RESPONSE TO BOLUS INJECTION OF PHENYLEPHRINE IN ATROPINIZED PATIENTS

The changes of arterial pressure promoted by bolus injection of 50 mg phenylephrine (PHE) were studied in 20 atropinized patients (5 normal subjects, 13 patients with mitral valve disease, 1 patient with essential arterial hypertension and 1 patient with hypertrophic cardiomyopathy) submitted to routine catheterism. Patients with aortic valve disease, left ventricular outflow tract obstruction and intracardiac shunt were excluded from the study. All patients were in sinus rhythm, without heart failure. Arterial pressure started to increase at 14.8 +/- 5.4 s (range, 5.6 to 27 s; mean +/- SD) after PHE. There was an increase of 37.8 +/- 16.7 mmHg (range, 12.5 to 70 mmHg) in systolic pressure and of 26.6 +/- 11.1 mmHg (range, 7.5 to 42.5 mmHg) in diastolic pressure. Peak hypertension was attained at 36.6 +/- 16.4 s (range, 10.8 to 64.9 s) and hypertension continued for 176 +/- 92 s (range, 11 to 365 s). Heart rate was 114 +/- 21 bpm before PHE and 111 +/- 21 bpm (P<0.05) after PHE. There were no adverse events associated with intravenous PHE injection in any patient, in accordance with the general view that bolus injection of PHE is a safe and practical maneuver to promote arterial hypertension.

Arterial-hypertension in the elderly

The authors review the epidemiology, the etiological factors, the effect of the treatment in the evolution of the cardiovascular disease in arterial hypertension in elderly, and the use of angiotensin-converting-enzyme inhibitors such as a treatment option.

Studies of natural-killer-cells in pregnancy-induced hypertension

The number and activity of natural killer (NK) cells were studied in 20 patients with pregnancy-induced hypertension (PIH), 15 uncomplicated pregnant women and 16 healthy non-pregnant women, All the pregnant women were primigravidae and were evaluated during the third trimester of gestation. Peripheral blood NK cells were detected with monoclonal antibodies by indirect immunofluorescence and cytotoxic activity was measured using a single-cell assay against K562 target cells. Hypertensive pregnant women had an increased number of circulating NK cells associated with a significant decrease of NK activity, the cytotoxic activity was significantly lower in normal pregnant and PIH women when compared with non-pregnant controls. The onset of immature NK cells in peripheral blood and the impairment of their cytotoxic activity in PIH patients may be associated with hormones and immunosuppressive substances produced by tissues occurring at the maternal-fetal interface.

Endothelial dysfunction in DOCA-salt hypertension - Possible involvement of prostaglandin endoperoxides

The effects of the arachidonic acid metabolism inhibitors on the acetylcholine responses of aortae from control (CR) and deoxycorticosterone acetate (DOCA)-salt hypertensive (HR) rats were investigated. The acetylcholine decreased response observed in HR [relaxation (%): CR 95.5 +/- 2.7, n = 4; HR 52.0 +/- 6.3, n = 5, p < 0.05] was restored by the cyclooxygenase inhibitor piroxicam [relaxation (%): CR 99.8 +/- 0.2, n = 4; HR 86.0 +/- 4.0, n = 5] and by the thromboxane synthetase inhibitor and the thrombox ane A(2)/prostaglandin H-2 receptor antagonist ridogrel [relaxation (%): CR 92.1 +/- 4.4, n = 7; HR 93.1 +/- 2.0, n = 7] but not by the inhibitors of thromboxane synthetase, prostacyclin synthetase, cytochrome P-450 monooxygenase, and lipoxygenase. So, endoperoxide intermediates seem to be involved in the decreased endothelium-dependent relaxation to acetylcholine in DOCA-salt hypertension. (C) 1999 Elsevier B.V. All rights reserved.