Nephrectomy modifies renal angiotensin II effects in kidney donors.

BACKGROUND: Age, gender, menopausal status, a family history of hypertension, and renal vascular response to angiotensin II are involved in the progression of renal failure from its very beginning. METHODS: In order to investigate their importance on this progression, we measured effective renal plasma flow (ERPF) and glomerular filtration rate (GFR), and calculated glomerular pressure (Pglo) and afferent and efferent arteriole resistances (by means of Gomez formulae) in 26 normotensive kidney donors before and after nephrectomy. RESULTS: Renal reactivity to angiotensin was the only variable that affected changes in renal and glomerular hemodynamics after the loss of renal tissue: in subjects with greater angiotensin reactivity, higher afferent resistances (Ra) and lower glomerular filtration and pressure before nephrectomy change to higher efferent resistances (Re) and higher Pglo and filtration after nephrectomy. CONCLUSIONS: In normotensive donors with a normal compensatory response to nephrectomy, baseline renal reactivity to angiotensin II can influence renal and glomerular hemodynamics 1 year after nephrectomy.

[Behavior of post-occlusion systolic blood pressure after long duration blockade. Effect of induced hypertension]. / Verhalten des postokklusiven systolischen Blutdrucks nach langdauernder Sperre. Effekt einer induzierten Hypertension.

A suprasystolic blockade (300 mm Hg) was applied for 50 to 60 min to the thigh of the affected leg with a blood pressure cuff in 13 patients with occlusions of the femoral artery. Afterwards, the pre-postocclusive systolic pressure difference was clearly less in most patients than before the compression manoeuvre. This reduction of the systolic pressure gradient, which was greatest in the first hour and slowly decreased in subsequent days, is likely to be based on a dilatation of the collateral arteries. The reaction was especially pronounced in patients with isolated occlusion of the femoral artery. Since the entire collateral circulation is largely in the region of the cuff compression in these cases, the collateral dilatation might arise from the powerful and long lasting pressure. In 9 patients it was investigated whether an increase of systemic blood pressure induced by hypertension can be transduced more effectively to the postocclusive arterial system when the collateral arteries are "paralyzed". The heterogeneous results show that such an effect can evidently only be expected when the collateral circulation is restricted to the thigh. However, such conditions are probably not usual in poorly compensated stage IV following Fontaine, in which a temporary peripheral increase of blood pressure is likely to be reasonable for therapy.

[Character of arterial pressure changes under combined action of pressor and depressor agents]. / Kharakter izmenenii arterial'nogo davleniia pri sochetannom deistvii pressornykh i depressornykh veshchestv.

It is shown in acute experiments in cats that byphasic arterial pressure changes occurred due to action of two heterodirectional and equivalent humoral stimuli. Magnitudes of both initial depressor and following pressor phases were authentically less than the ones due to separate action of those stimuli. It is noticed that the character of sum reaction depends neither on action mechanisms of vasoactive agents in the blood circulation system nor differences in the latent period of the effect of those drugs, but connected with intensiveness of stimuli. Predominance of depressor phase magnitude was shown to observe due to a rise of stimuli intensiveness down to complete disappearance of pressor reaction.

Duration of delayed-type autoimmunity against arterial vessel-wall antigens following acute hypertensive damage to arterial vessels in rats.

Acute hypertensive damage to small arteries and arterioles in rats was induced by intravenous injections of Hypertensin. The in vitro immunological method of the agarose migration technique was used to demonstrate delayed-type autoimmunity against arterial vessel-wall antigens. By this technique the autoimmunity could be demonstrated for about 16 weeks after the acute hypertensive damage to the arterial vessels. The results of the autoimmunity were given as migration indices. These were lowest during the first 4-5 weeks after the damage to the vessels whereupon they showed higher and higher values, and finally the migration indices were identical with those of the control rats after about 16 weeks.

[Metabolism of angiotensin II during angiotensin infusion and following sodium depletion]. / Angiotensin II-Stoffwechsel bein Angiotensininfusion und bei Kochsalzentzug

1. Angiotensin II (A II) and angiotensin (3--8)-hexapeptide (H) were measured by radioimmunoassay in arterial and venous plasma before and during infusion of angiotensin II-amide in five normotensive subjects, both in sodium-replete and sodium-depleted states. The separation of the oligopeptides was performed by thin layer chromatography. 2. Before sodium-depletion the mean ratio of arterial to venous A II was 1.14+/-0.11:1, corresponding to an A II-extraction of approximately 12% during a single forearm passage. Infusion of A II-amide increased extraction of A II. The mean ratio of arterial to venous A II increased to 1.68+/-0.3:1, corresponding to an extraction of approximately 39% when 8 ng-min-1-kg-1 were infused. 3. Sodium depletion increased arterial and venous concentrations of A II and H. During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion. The extraction of A II did not differ significantly in both states. 4. The augmented extraction extraction of A II observed during infusion of angiotensin II-amide suggest an overproportional increase of the metabolism of A II under the latter condition. Sodium depletion, however, does not appear to cause a percent change in A II metabolism.