SUMMARY1. Action potentials were recorded from slips of the cervical vagi in anaesthetized dogs and rabbits. Single functional units with atrial patterns of discharge (Paintal Type A, B and intermediate) were obtained and then attempts were made to alter (i.e. convert) their patterns of discharge. Finally the points of origin of these action potentials were located.2. Thirty unselected units were investigated in thirty dogs. Twentyseven of these were located in the endocardium of the vein-atrial system and the ratio of the type A, type B and intermediate type receptors was 1: 16: 10; three units were located elsewhere in the chest. Conversion of the pattern of discharge was achieved in twenty of the twenty-seven units; conversion was achieved in the single type A unit.3. In a second series of experiments in dogs, eight Paintal Type A units were selectively studied in fifteen animals. Four of these were located in the endocardium and all were converted. The remaining four were located outside the endocardium and conversion could not be achieved in two of these. Thus in the entire investigation, the 'type A' units which could not be converted were all located at sites other than the atrial endocardium.4. In the corresponding unselected study in the rabbit, eleven units were studied in eleven animals. Nine of these units were located in the atrial endocardium and the ratio of the type A, type B and intermediate type receptors was 2:1:6. Conversion was achieved in both type A units, the sole type B unit and two of the intermediate units.

Plasma volume and blood volume were measured using T‐1824 in two groups of dogs which were kept on a diet differing only in its content of sodium chloride for periods exceeding six weeks. The group on low sodium intake received 0·55 mmol Na+.kg‐1.day‐1 and the group on high sodium intake received 12·4 mmol Na+.kg‐1.day‐1. Both plasma and blood volumes were distinctly greater in the group on high sodium intake than those in the group on low sodium intake, and there was no difference in the haematocrit between the two groups of dogs. It is concluded that a greater plasma volume and red cell volume resulted from high sodium intake than from low sodium intake.

1. The effects of intracoronary bolus infusion of hypertonic saline solution on left circumflex coronary blood flow were examined in sixteen anaesthetized and artificially ventilated pigs whilst preventing changes in heart rate and arterial blood pressure. 2. In fourteen pigs, bolus infusion of 7 5% hypertonic saline solution (2 ml within 30 s) caused a steady-state increase in coronary blood flow without significantly affecting right atrial or left ventricular pressure and its rate of rise (dP/dtmax). Infusing nornial saline solution (0 9 %) at the same rate and volume in seven pigs did not have this effect. 3. In five pigs, the magnitude and the duration of the response of increase in coronary blood flow were increased in a graded manner by graded increases in the concentration of the hypertonic saline solution between 2-5, 5 and 7-5 %. 4. In nine pigs, the response of increase in coronary blood flow to the bolus infusion of hypertonic saline solution was not affected by the blocking agents atropine, propranolol and phentolamine, but it was completely abolished in the same nine pigs by the subsequent intracoronary administration of NW-nitro-L-arginine methyl ester (L-NAME) which blocks the synthesis of endothelium-derived relaxing factor (EDRF) and in seven pigs by solely giving L-NAME. 5. These results showed that the intracoronary bolus infusion of hypertonic saline solution in anaesthetized pigs caused a coronary vasodilatation which involved mechanisms dependent on the release of EDRF.Intravenous administration of small volumes of 7 5% hypertonic saline solution (2400 mosmol F-') has been used as a rapid treatment for hypovolaemic shock in animals and in man

This study was undertaken to determine the effects of progesterone on the peripheral circulation. In prepubertal female pigs anesthetized with sodium pentobarbitone, changes in the superior mesenteric, left renal and left external iliac flow caused by intravenous infusion of progesterone were assessed using electromagnetic flow meters. Changes in heart rate and arterial blood pressure were prevented by atrial pacing and by connecting the arterial system to a pressurized reservoir containing Ringer solution. In 20 pigs, infusion of 1 mg/kg of progesterone increased mesenteric, renal and iliac flow. In a further 4 pigs, the vasodilatory effects of the hormone were enhanced by graded increases in the dose between 1, 2 and 3 mg/kg. The mechanisms of these responses were studied in the 20 pigs by repeating the experiment after hemodynamic variables had returned to the control values before infusion. In 5 pigs, blockade of adrenergic receptors with propranolol and phentolamine did not affect the responses elicited by progesterone. The increases in mesenteric, renal and iliac flow to progesterone were prevented, respectively, by the injection of N^ω-nitro-L-arginine methyl ester into the mesenteric (5 pigs), the renal (5 pigs) or the iliac artery (5 pigs). The present study shows that intravenous infusion of progesterone dilated mesenteric, renal and iliac circulations. The mechanism of this response involved the release of nitric oxide.

SUMMARYTo determine whether distension of the urinary bladder reflexly affects coronary blood flow, experiments were performed in eleven dogs anaesthetized with sodium pentobarbitone. Both ureters were cannulated and the urinary bladder was distended with warm Ringer solution at a steady intravesical pressure. Arterial blood pressure was prevented from changing by a pressurized reservoir of warm Ringer solution connected to the femoral arteries. Coronary blood flow was measured with an electromagnetic flowmeter positioned around the origin of the left circumflex coronary artery. When the reflex increase in heart rate was prevented by atrial pacing in seven dogs, distension of the urinary bladder always caused a decrease in mean coronary blood flow. Similar results were obtained in all eleven dogs after administration of propranolol. The decrease in mean coronary blood flow was significantly reduced by atropine or bilateral cervical vagotomy, and was abolished by bretylium tosylate. The results showed that distension of the urinary bladder reflexly decreased mean coronary blood flow, a response involving efferent cardiac vagal and sympathetic pathways.

Insulin can influence the vasculature by a sympathetically mediated vasoconstriction and a vasodilatation; the latter effect predominates in the renal circulation of anesthetized pigs. We determined the effect of intravenous infusion of insulin on coronary blood flow in pentobarbitone-anesthetized pigs at constant heart rate, arterial pressure and blood levels of glucose and potassium. In 6 pigs, infusion of 0.004 IU kg^–1 min^–1 of insulin decreased coronary flow despite increasing left ventricular dP dt_max^–1; when the latter was abolished by propranolol, the coronary flow response was augmented. The mechanisms of this response were examined in 22 pigs given propranolol. Phentolamine changed coronary flow response to an increase (6 pigs) and this was abolished by intracoronary injection of N^ω-nitro-L-arginine methyl ester (L-NAME; 5 pigs). L-NAME augmented coronary flow response (6 pigs) and this was abolished by phentolamine (5 pigs). In 18 pigs given propranolol, three incremental doses of insulin caused graded coronary flow decreases whether L-NAME was given (6 pigs) or not (6 pigs) beforehand, and caused graded coronary flow increases after phentolamine (6 pigs). Thus insulin caused a coronary vasoconstriction mediated by sympathetic α-adrenergic effects and a vasodilatation related to the release of nitric oxide. The net effect was a coronary vasoconstriction.

Dehydroepiandrosterone has been implicated in vascular disease and its associated insulin resistance and hypertension, though little is known about its vascular effects. We have recently shown in prepubertal anaesthetized pigs that intravenous infusion of dehydroepiandrosterone caused coronary vasoconstriction through the inhibition of a vasodilatory β-adrenergic receptor-mediated effect related to the release of nitric oxide. The present study was designed to investigate the effect of dehydroepiandrosterone on mesenteric, renal and iliac vascular beds. In prepubertal pigs of both sexes anaesthetized with sodium pentobarbitone, changes in superior mesenteric, left renal and left external iliac blood flow caused by intravenous infusion of dehydroepiandrosterone were assessed using electromagnetic flowmeters. Changes in heart rate and arterial blood pressure were prevented by atrial pacing and by connecting the arterial system to a pressurized reservoir containing Ringer solution. In 22 pigs, infusion of 1 mg h −1 of dehydroepiandrosterone decreased mesenteric, renal and iliac blood flow. In a further 10 pigs, dose-response curves were obtained by graded increases in the infused dose of hormone between 0.03 and 4 mg h −1 . The mechanisms of the above response were studied in the 22 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. Blockade of α-adrenoceptors with intravenous phentolamine (five pigs) did not affect the dehydroepiandrosterone-induced mesenteric, renal and iliac vasoconstriction. This response was abolished by blockade of β 2 -adrenoceptors with intravenous butoxamine (five pigs) and by blockade of mesenteric, renal and iliac nitric oxide synthase with intra-arterial administration of N ω -nitro-L-arginine methyl ester (seven pigs), even after reversing the increase in local vascular resistance caused by the two blocking agents with intravenous infusion of papaverine. In five pigs, the increase in measured blood flow caused by intravenous infusion of isoproterenol (isoprenaline) was significantly reduced by infusion of dehydroepiandrosterone. The present study showed that intravenous infusion of dehydroepiandrosterone primarily caused mesenteric, renal and iliac vasoconstriction. The mechanisms of this response were shown to be due to the inhibition of a vasodilatory β 2 -adrenergic receptor-mediated effect, which possibly involved the release of nitric oxide. Dehydroepiandrosterone is a principal C-19 adrenal steroid whose plasma levels significantly increase following puberty, but decline with advancing age (Parker, 1999). There has been a controversy as to whether or not this hormone is involved in the development of vascular disease (LaCroix et al. 1992;Nestler et al. 1992;Herrington, 1995;Alexandersen et al. 1996;Khaw, 1996;Porsova-Dutoit et al. 2000), insulin resistance, obesity and hypertension (Nestler et al. 1992;Ebeling & Koivisto, 1994; BarrettConnor & Goodman-Gruen, 1995a,b;Fuenmayor et al. 1997;Suzuki et al. 1999;Kr...

SUMMARYThe diuretic response to stimulation of left atrial receptors, by distending balloons located either at the pulmonary vein-left atrial junctions or in the body of the left atrium, was studied during blockade of the generation of angiotensin II using a continuous infusion of angiotensin converting enzyme inhibitor, SQ 14,225, in anaesthetized dogs. Despite blockade of angiotensin conversion, known also to potentiate the activity of bradykinin, a diuretic response was obtained in each dog; the response was similar to that observed in dogs without blockade of angiotensin conversion. Angiotensin II and bradykinin did not significantly influence the rate of secretion of Malpighian tubules of Rhodnius prolixus, which have been shown capable of detecting the blood-borne agent known to mediate the diuretic response. It is concluded that neither angiotensin II nor bradykinin is likely to be the blood-borne agent released by stimulation of atrial receptors.