Publications by authors named "J Rudenstam"

Aims: Renal medullary blood flow is important in blood pressure regulation and is surprisingly unaffected by the vasoconstrictor action of angiotensin II (Ang II). This study tested if the effect of Ang II on the renal papillary circulation is modulated by bradykinins, prostaglandins or NO (NO). In anaesthetised Wistar rats, total renal blood flow (RBF) was measured, as was cortical (CBF) and papillary (PBF) blood flow, using the laser-Doppler technique, in responses to Ang II (30 ng kg(-1) min(-1)) alone and after ACE inhibition (enalapril) or bradykinin/prostaglandin synthesis inhibition (ketoprofen, aprotinin).

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Blood pressure (BP) is rapidly normalized when removing the obstruction from the renal artery of a two-kidney, one-clip renovascular hypertensive rat (unclipping). This study tested whether efferent renal nerve stimulation (ERNS) of the unclipped kidney affects this drop in BP or the associated changes in diuresis-natriuresis and regional renal blood flow. Three groups of anesthetized renovascular hypertensive Wistar rats were studied: 1) W(C) (time control); 2) W(UC) (unclipped after 30 min); and 3) W(UC+NS) (unclipped after 30 min, with ERNS at 5 Hz for 2 h).

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It has long been recognised that the kidneys take part in blood pressure control via both their exocrine and endocrine functions. An endocrine antihypertensive function of the renal medulla has been proposed. The renal medullary depressor substances ("medullipins"), are released in response to increased renal perfusion pressure.

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Chemical renal medullectomy with 2-bromo-ethylamine hydrobromide (BEA) has been used to study the importance of the renal medulla in blood pressure regulation. However, conclusive evidence as to whether BEA treatment affects the glomerular barrier is lacking. In the present study, the effects of BEA upon glomerular permselectivity for albumin were studied using isolated kidneys (IPK) perfused at a low temperature (8 degrees C) to inhibit tubular reabsorption of proteins.

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The threshold for activation of the humoral renal antihypertensive system, presumably residing in the renomedullary interstitial cells (RIC), is substantially reset upwards in the spontaneously hypertensive rat (SHR). Depressor reactions, normally elicited by an increased renal perfusion pressure, can be inhibited either by high frequency renal nerve stimulation or blockade of nitric oxide synthesis, i.e.

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