摘要:

Systemic administration of acetazolamide (ACZ) causes glomerular filtration rate (GFR) to fall. Clearance and micropuncture experiments were done to define the mechanism of this drug effect. When rats were infused with ACZ intravenously, kidney GFR fell by 30% and single nephron (SN) GFR (measured by collecting distal tubule fluid) fell by 23%. Changes in arterial blood pressure, arterial pH, extracellular fluid volume, and proximal tubule pressure were not sufficient to account for the decrease in GFR. When SNGFR was measured by collecting proximal tubule fluid, with the loop of Henle having been blocked for 2–5 min, SNGFR was higher than the distally measured value and was not different than control. The results are consistent with the fall in GFR being caused by activation of the tubulo‐glomerular feedback mechan

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06945.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb00001.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

摘要:

The change in renal nerve activity under conditions known to increase renal sodium excretion was studied. In adult Sprague Dawley rats, anaesthetized with Inactin®, nor‐motonic and hypertonic NaCl solutions were infused into 1) a vein, 2) a carotid artery and 3) the third ventricle. The left kidney was freed and placed in a plastic cup. A renal nerve was dissected free and placed on a stainless bipolar electrode. The nerve was cut distal to the electrode. The nerve signals were amplified and recorded on a tape recorder. Simultaneously integrated nerve signals and also arterial and venous pressures were recorded. Intracarotid infusion of a 1 M NaCl solution increased sodium output and temporarily decreased renal nerve activitv by some 35%. Corresponding intravenous (i.v.) infusion gave an increase in renal nerve activity and also in sodium output. The latter increase was delayed compared with that caused by the intracarotid infusion. No variations in blood pressure were noted. In control experiments with a slow i.v. infusion of physiological saline, renal nerve activity increased throughout the experiment, while sodium excretion remained constant. During infusion of a 1 M NaCl solution into the third ventricle, renal nerve activity decreased in about half of the cases. This reduction was often accompanied by an increased arterial blood pressure and an increased sodium output. Arterial blood pressure increases were especially pronounced at the highest infusion rate, i.e. 800 nl‐min‐1. Isotonic volume expansion of 2% of the body weight resulted in a transient decrease in renal nerve activity by about 30%. Venous blood pressure rose and sodium output increased six‐fold. The decrease in nerve activity was observed both when the vagal nerves were intact and when they

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06946.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb00002.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

摘要:

Small doses of insulin (1.25 U/kg) had no effect on the serum gastrin concentration but stimulated gastric acid secretion in contrast to what was the case in unoperated rats. Glucose prevented the acid response to insulin. The gastric histidine decarboxylase was not activated by insulin following antrectomy. In vagally denervated rats, insulin (5 U/kg) increased the serum gastrin concentration slightly but did not raise the histidine decarboxylase activity. We interpret the results as follows: With small doses of insulin the gastric secretagogue effect is attributable mainly to vagal nerve stimulation evoked by the hypoglycemia. With large doses of insulin there is no acid response. The effects on the parietal cells of the ensuing hypergastrinemia are counteracted by an unknow mechanism, which however does not prevent gastrin from releasing gastric histamine and stimulating gastric histidine decarboxylase. The insulin‐induced release of gastrin is not elicited exclusively through vagal excitation by hypoglycemia, since insulin releases gastrin also after vagotomy and after glucose administration. The great enzyme‐activating effect of insulin is a consequence of gastrin release. In addition, however, insulin seems to enhance the responsiveness of the enzyme‐containing cells to gastrin. Insulin is a poor substitute for vagal excitation in that it exerts a number of actions which are unrelated to v

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06947.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

摘要:

Local and remote regulation of subcutaneous blood flow in the forearm and leg was studied during head‐up tilt (45°) in 6 young healthy male subjects. Relative blood flow was estimated by the local133Xe washout technique. Lowering of a leg lead to a 51 % decrease in its subcutaneous blood flow due to a veno‐arteriolar reflex elicited by the increase in venous transmural pressure. During head‐up tilt subcutaneous blood flow in the arm remaining at heart level decreased by 27%, in the leg blood flow decreased by 50%. Following proximal nervous blockade, head‐up tilt did not induce vasoconstriction in forearm at heart level, but blood flow in distal leg decreased by 45%. Thus there was no difference in the vasoconstrictor response in the leg to head‐up tilt or lowering of the labelled area by 40 crn. Since head‐up tilt caused neurogenically mediated vasoconstriction in subcutaneous tissue, subcutaneous blood flow in the extremities seems to be regulated by remote (baroreceptor) as well as local sympathetic reflex mechanisms (veno‐arte

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06948.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

摘要:

The relation between plasma osmolality (pOsm) and the concentration of immunoreactive vasopressin in plasma from an external jugular vein (pAVP) was studied in dogs prepared with carotid loops and anesthetized with chloralose‐pentobarbital. Control meail pAVP was 0.6–1.0 μU/ml, after 24 h of dehydration pAVP was tripled. Isosmotic volume expansion for 10 min elicited a decrease in pAVP in all cases not associated with low control values of pAVP. I.v. hyperosmotic infusions (A pOsm: 9 or 18 mOsm/kg in 10 min) increased pAVP. No significant alterations in pAVP occurred in relation to infusions during which the head or the remainder of the body was selectively supplied by hyperosmotic blood. Statistically, the distribution of the pAVP values suggests the existence of two populations, in euhydrated animals high concentrations (>8 μU/ml) were found in a small fraction of the samples. It is concluded that (i) in chloralose‐anesthetized, non‐traumatized dogs pAVP is very similar to values found in venous plasma from conscious dogs, (ii) the pAVP measurements support the concept of an episodic secretion of vasopressin, and (iii) under the present circumstances, an ubiquitous increase in pOsm is a more effective stimulus for vasopressin release than a similar but selective increase in the osmolality of the blood flowing towards

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06949.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

摘要:

Verney's hypothesis of cerebral osmoreceptors controlling the renal excretion of water via vasopressin was reinvestigated in conscious trained dogs provided with bilateral skin loops containing the common carotid arteries. In multiple experiments in two dogs, bilateral intracarotid injections (0.25 ml.(kg b. wt.)‐1per artery in 10 s) of a hyperosmotic solution of sodium chloride (0.257 mol/l) during transient water diuresis failed to produce an antidiuretic response, although it is estimated that the injections elevated the osmolality of the carotid blood by 12–15%. In another 5 dogs, bilateral intracarotid infusions of hyperosmotic saline (45 μmol. (kg b. wt. min)‐1per artery for 10 min) during sustained water diuresis resulted in a 3% increase in jugular venous osmolality and an antidiuretic response without detectable changes in heart rate or mean arterial pressure. Equal intravenous hyperosmotic or intracarotid isosmotic infusions were not associated with antidiuretic responses. Analysis of the concomitant concentrations of vasopressin in plasma fell short of supporting the hypothesis that the antidiuretic response to intracarotid hyperosmotic infusions was exclusively or mainly due to liberation of vasopressin. although the renal response could be mimicked by exogenous vasopressin. It is concluded that the present results—although discordant with several of Verney's results and assumptions—nevertheless support the concept of a cerebral solute receptor influencing the rate of renal water

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06950.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

摘要:

The cross reactivity of two currently used substance P (Sp) antisera (K 16 and K 25) with various analogues of SP, partial sequences of SP and other naturally occurring peptides were tested in a radioimmunoassay system. Both antisera were found to be C‐terminal directed, this tendency being most pronounced for antiserum K16. The capacity of antiserum K 25 to bind various SP‐related peptides correlated to the previously described biological activity of these peptides on the isolated guinea pig ileum. The results thus indicate that this antiserum binds to a biologically active part of the SP‐mol

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06951.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY

摘要:

The effect of hypoxia and blood flow on the capillary permeability‐surface area product (PS) of51Cr‐EDTA was investigated in canine myocardium of open chest anesthetized dogs at constant aortic pressure, heart rate, and cardiac output. PS was determined by bolus injection of51Cr‐EDTA into the left anterior descending coronary artery (LAD) and external registration of the response curve. Vascular conductance (G) and PS were measured: (1) during pump perfusion of LAD with arterial blood (control state), and (2) during vasodilation obtained by LAD perfusion with deoxygenated blood at same blood flow as in control state, and (3) during increased blood flow with deoxygenated blood. Mean value of G in control state was 1.31 ml. min‐l. (100 g)‐1(mmHg)‐1. The ratio G‐hypoxialG‐control used to assess the extent of vasodilation was 2.42 (range 1.67–3.56) during hypoxia and unchanged flow and 2.82 (range 1.81447) during hypoxia and increased flow. Mean value of PS in control state was 36 ml. (100 g)‐1. min‐1. With maximum vasodilation and constant blood flow PS increased to 47.3 ml.(100 g)‐1.min‐1(37%) and during increased blood flow to 69.0 ml.(100 g)‐1. min‐1(96%). The increase in PS most likely reflects an increase in capillary surface area available for exchange of51Cr‐EDTA indicating a 1.4– to

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1982.tb06952.x

出版商:Blackwell Publishing Ltd    

年代:1982

数据来源: WILEY