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D J Ramsay

Publications and source records attributed to D J Ramsay.

At least 37 records · Page 2Linked to original sources
PubMed1986

Effects of sodium depletion and angiotensin II on osmotic regulation of vasopressin.

After alterations in sodium balance, osmotic reactivity of vasopressin (AVP) release was evaluated in seven conscious dogs during bilateral intracarotid infusions of hypertonic saline. A low-sodium diet reduced plasma sodium concentration by 3%; deoxycorticosterone acetate (30 mg/day for 2 days) elevated the concentration by 1%. Neither treatment altered resting plasma AVP. Hypertonic intracarotid infusions increased jugular plasma osmolality by 20 +/- 2 mosmol/kg independent of manipulations. Plasma AVP values were significantly increased (P less than 0.05) in sodium-depleted dogs compared with values of the control animals. In addition, the osmotic reactivity of AVP release was evaluated during exogenous administration of angiotensin II (ANG II). Intravenous infusion of ANG II (5 ng . kg-1 . min-1) increased plasma concentration of ANG II but did not alter concentration of plasma AVP. The slope for the relationship of jugular plasma osmolality to plasma AVP during hypertonic intracarotid infusions was significantly increased with intravenous infusion of ANG II. Sodium depletion and intravenous ANG II potentiate the relationship of plasma osmolality and plasma AVP when evaluated with intracarotid hypertonic saline infusions in dogs.

Angiotensin II↗
PubMed1986

Endocrine mechanisms regulating sodium excretion during water deprivation in dogs.

The time course and mechanism of the natriuresis that accompanies 24 h of water, but not food, deprivation were studied in eight chronically catheterized dogs. Dogs were fed a controlled diet containing 35 meq of sodium, 110 meq of potassium, and 107 ml of water at 9:00 A.M. every day (time 0), and urine and blood samples were taken at 0, 2, 4, 6, 8, 10, 12, 16, 20, and 24 h after feeding on 3 consecutive days: the control, dehydration, and recovery days. Twenty-four hours of water deprivation decreased body weight by 880 g, increased plasma sodium by 7.2 meq, and increased plasma osmolality by 22.5 mosmol/kg. Cumulative daily sodium excretion increased from 30.4 +/- 2.8 meq on the control day to 50.7 +/- 5.7 meq on the dehydration day (P less than 0.01) and resulted in significant negative sodium balance that developed during the last half of the dehydration day. Cumulative sodium excretion during the first half of the dehydration day was not different from the corresponding period of the control day. Cumulative potassium excretion also increased from 91.9 +/- 4.5 meq during the control day to 123.0 +/- 6.7 meq during the dehydration day (P less than 0.01). Significant and progressive increases in plasma vasopressin concentration and renin activity were observed during water deprivation, but plasma aldosterone did not change from control levels. Furthermore, there was no correlation between the rate of sodium excretion and plasma vasopressin or aldosterone concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1986

Cardiac receptors, vasopressin, and corticosteroid release during arterial hypotension in dogs.

The relative roles of cardiopulmonary and sinoaortic baroreceptors in the regulation of vasopressin and corticosteroid release were evaluated in conscious dogs. The dogs were prepared with inflatable cuffs around either the ascending aorta, proximal to the brachiocephalic trunk, or the pulmonary artery. Inflation of the cuffs was adjusted to cause a reduction of mean systemic arterial pressure (MAP) of 0, 5, 10, 20, or 30% of control for 1 h in separate experiments. In spite of the profound systemic hypotension caused by constriction of the ascending aorta, plasma vasopressin failed to increase and corticosteroids increased only in response to a 30% decrease in MAP. In contrast, a 5% reduction in MAP during pulmonary arterial constriction increased plasma vasopressin and corticosteroid concentrations significantly. The apparent paradox in these results is correlated with different effects of the two maneuvers on left atrial pressure. Left atrial pressure increased dose dependently during inflation of the ascending aortic cuff but decreased during inflation of the pulmonary arterial cuff. In contrast, graded inflation of the pulmonary arterial cuff caused dose-dependent increases in right atrial pressure, plasma vasopressin, and corticosteroids. Therefore, we conclude that powerful inhibitory signals, arising from the left heart, can inhibit vasopressin and hypotension release in response to systemic hypotension.

Adrenal Cortex Hormones↗
PubMed1986

Increased right or left atrial pressure stimulates release of atrial natriuretic peptides in conscious dogs.

To compare release of immunoreactive atrial natriuretic peptides (iANP) caused by distention of the right and left atria, dogs were prepared with occluding cuffs around either the ascending aorta (n = 5) or the pulmonary artery (n = 4). Graded inflation of the ascending aortic cuff for 60 min caused increments in left atrial pressure (LAP) but no change or a decrease in right atrial pressure (RAP). Plasma iANP increased significantly (P less than 0.01) in response to increases in LAP as small as 2.9 +/- 0.4 mmHg. There was a significant correlation between the increment in LAP and the rise in plasma iANP (r = 0.64, n = 25, P less than 0.01). Graded inflation of the pulmonary artery cuff caused increments in RAP and a fall in LAP. Plasma iANP increased significantly (P less than 0.01) in response to increases in RAP as small as 2.8 +/- 1.1 mmHg. Also, there was a significant correlation between the increments in RAP and the rise in plasma iANP (r = 0.69, n = 20, P less than 0.01). These results indicate that physiologic increases in either RAP or LAP is sufficient to cause increased plasma levels of iANP in conscious dogs.

Animals↗
PubMed1985

Mechanism of inhibition of renin secretion by increased left atrial pressure.

Experiments were designed to elucidate the mechanism of the failure of systemic hypotension to stimulate renin release in the presence of elevated left heart pressure. We conducted a series of graded ascending aortic and suprarenal cuff inflations in dogs with bilateral renal denervation (n = 5). The renal perfusion pressure (RPP) was reduced by 10, 20, and 30% of control by inflation of either cuff. Comparison of the renin response with inflation of the ascending aortic to the suprarenal cuff revealed a clear increase in the threshold required to elicit a renin response to graded reduction of RPP after inflation of the ascending aortic cuff. These results may be explained by differential effects of the two maneuvers on left heart pressure. Left atrial pressure increased during inflation of the ascending aortic cuff but did not change during inflation of the suprarenal cuff. Since the kidneys were denervated, the shift in threshold must be caused by a humoral substance(s). In conclusion, our findings suggest that the efferent pathway of potent inhibition of renin release from the left heart is mediated, at least partially, by a humoral substance.

Angiotensin I↗
PubMed1984

Sodium balance and aldosterone during dehydration and rehydration in the dog.

The regulation of sodium metabolism and the renin-angiotensin-aldosterone system was evaluated during 24 h of water, but not food, deprivation and during rehydration in the dog. Dehydration caused increases in plasma concentrations of sodium (6.0 +/- 0.7 meq/l), protein (0.8 +/- 0.1 g/dl), vasopressin (5.3 +/- 0.9 pg/ml), and renin activity (3.5 +/- 1.1 ng AI X ml-1 X 3 h-1). Plasma aldosterone was unchanged and plasma potassium fell slightly (0.2 +/- 0.1 meq/l). During dehydration, food, and thus sodium intake fell by more than 10% in 12 of 19 dogs, but urinary sodium excretion increased significantly, leading to a negative sodium balance (1.9 +/- 0.2 meq/kg). Sodium retention was observed after rehydration and sodium balance; plasma electrolytes, vasopressin, and plasma renin activity (PRA) returned turned to control levels after the 1st day of recovery. However, plasma aldosterone was slightly elevated at this time, returning to control after the 2nd day of recovery. The dehydration-induced natriuresis could not be accounted for by a fall in plasma aldosterone. However, sodium retention following rehydration could be aldosterone dependent, because additional studies showed a threefold rise in plasma levels of the hormone 1 h after drinking. The acute rise in aldosterone correlated closely (r = 0.82) with the fall in plasma sodium after drinking but not with changes in adrenocorticotrophic hormone, PRA, or plasma potassium. It is concluded that natriuresis is a homeostatic response to dehydration as a means of ameliorating the rise in body fluid osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1984

Elevated cardiac pressure inhibits renin release after arterial hypotension in conscious dogs.

The relative roles of cardiopulmonary, sinoaortic, and renal baroreceptors in the regulation of plasma renin activity (PRA) were evaluated in dogs with chronically implanted cuffs around the ascending aorta proximal to the brachiocephalic artery, the abdominal aorta just proximal to both renal arteries, or both. Inflation of either cuff was adjusted to cause a reduction of distal arterial pressure and hence renal perfusion pressure (RPP) of 0, 5, 10, 20, or 30% of control for 1 h. Reduction of RPP by inflation of the suprarenal cuff (n = 4) led to a significant (P less than 0.05) increase in PRA throughout the dose range examined. However, constriction of the ascending aorta (n = 7) to cause identical reductions in RPP failed to increase PRA. The apparent paradox in these results may be explained by differential effects of the two maneuvers on left atrial pressure. Left atrial pressure increased dose dependently during inflation of the ascending aortic cuff but did not change during inflation of the suprarenal cuff. To determine if elevated right atrial pressure (RAP) would inhibit renin release after systemic hypotension, another group of dogs (n = 4) was prepared with cuffs around the pulmonary artery. Inflation of the pulmonary cuff to cause similar systemic hypotension led to significant (P less than 0.05) increases in PRA and RAP. Therefore we conclude that powerful inhibitory signals, arising from the left heart, can inhibit renin release in response to systemic hypotension.

Animals↗
PubMed1984

The defence of plasma osmolality.

The studies reported in this abstract are the result of various tests of osmosensitivity and sodium sensitivity on drinking, vasopressin secretion and sodium excretion in dogs before and after discrete lesions of the OVLT. A successful lesion was defined as destruction of 95% of the OVLT without significant damage to periventricular tissue. Destruction of the OVLT elevated the threshold increase in plasma osmolality required to elicit drinking to intravenous infusion of hypertonic NaCl from 8 +/- 2 to 23 +/- 2 mosmol/kg H2O, and reduced water intake at these threshold osmolalities from 43 +/- 4 to 15 +/- 3 ml/kg. The water intake following 24 h of water, but not food, deprivation was 36 +/- 7 before the lesion and 43 +/- 9 ml/kg following, volumes which did not differ statistically. However, the effect of 24 h water deprivation on plasma osmolality and sodium excretion was altered by OVLT lesions. In control dogs, water deprivation increased plasma osmolality from 301 +/- 2 to 308 +/- 2 mosm/kg, plasma vasopressin from 2.0 +/- 0.3 to 6.8 +/- 1.3 pg/ml and plasma renin activity from 3.3 +/- 1.2 to 10.4 +/- 3.0 ng AI/ml/3 h and a natriuresis of 2 mEq of sodium/kg. Following OVLT lesions, water deprivation did not result in natriuresis. Furthermore, plasma osmolality increased from 314 +/- 7 to 331 +/- 6 mosmol/kg, vasopressin from 1.6 +/- 0.5 to 5.3 +/- 1.0 pg/ml and PRA from 9.6 +/- 2.4 to 18.2 +/- 5.4 ng AI/ml/3 h. The increase in plasma vasopressin was small in relation to the large rise in plasma osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1984

Hill plots of muscles bathed in hypertonic solutions.

The velocity of muscle contraction is found to decrease as the osmotic pressure increases for constant load. Vmax evaluated from computer fitted load/velocity curves shows two distinct activation processes when plotted against the reciprocal of absolute temperature. Hill's equation proves to be an accurate descriptor of the experimental P/V curves for each osmotic pressure and temperature. The area under the P/V curves was found to provide a more reliable parameter representing the overall muscle response than Vmax. When the bathing solution is made sufficiently hypertonic only one activation process remains. These effects are found to be reversible. The results are explained in terms of the inhibition of ATP splitting during the crossbridge power stroke.

Animals↗
PubMed1983

Inappropriate drinking and secretion of vasopressin after caval constriction in dogs.

The object of this study was to determine if chronic thoracic vena caval constriction affected mechanisms regulating water balance, independent of known changes in sodium metabolism in the dog. Fluid and electrolyte balances were determined for 5 days before and 14 days after constriction of the vena cava (n = 5) and in a separate population of time controls (n = 4). Cardiac output was reduced and heart rate was increased in response to chronic caval constriction although blood pressure was maintained at control levels. Water intake and plasma arginine vasopressin (AVP) increased from 31 +/- 4 ml/kg and 1.3 +/- 0.2 pg/ml during the control period to 81 +/- 6 ml/kg and 3.4 +/- 0.6 pg/ml during the period of caval constriction. The caval dogs developed a positive water balance, which preceded the development of a positive sodium balance. This led to a significant fall in plasma osmolality from a control mean of 296 +/- 1 to 284 +/- 4 mosmol/kg during caval constriction and dilutional hyponatremia. Plasma and blood volume increased significantly in response to constriction and were accompanied by formation of 123 +/- 10 ml/kg of ascitic fluid. These results show that water intake and plasma levels of AVP were increased in spite of a fall in plasma osmolality and an increase in vascular volume. These responses cannot be secondary to sodium retention because water was retained in excess of sodium hence hyponatremia. Therefore, chronic caval constriction causes a profound primary disturbance in mechanisms regulating water balance, which may contribute to the formation of edema fluid.

Adrenocorticotropic Hormone↗
PubMed1983

Role of volume and osmolality in the control of plasma vasopressin in dehydrated dogs.

Plasma vasopressin concentrations (pAVP) are elevated during dehydration due to alterations in extracellular fluid (ECF) volume and tonicity. The contributions of the reduction in volume and increase in plasma osmolality to the rise in pAVP were assessed in 6 dogs with bilateral carotid loops following 24 h of fluid, but not food, deprivation. Dehydration significantly (p less than 0.05) increased plasma osmolality from 297 +/- 1 to 315 +/- 2 mosm/kg), decreased body weight from 20.8 +/- 1.2 to 20.3 +/- 1.2 kg, and elevated pAVP from 1.4 +/- 0.2 to 5.3 +/- 0.6 pg/ml. The effect of extracellular fluid volume reduction was tested by reexpanding this compartment in dehydrated dogs with 0.15 M NaCl. Plasma vasopressin concentration was significantly reduced by 1.3 +/- 0.2 pg/ml (33 +/- 4%) and plasma osmolality unchanged following volume replacement. The contribution of the increase in plasma osmolality was assessed by bilateral intracarotid infusions of water at 0.6 ml/min/artery which lowered jugular venous plasma osmolality to euhydrated values (296 +/- 4 mosm/kg), but did not significantly reduce systemic plasma osmolality. Plasma vasopressin levels were significantly reduced 3.2 +/- 1.1 pg/ml (70 +/- 5%). Thus, following 24 h of fluid deprivation in dogs, the rise in pAVP is due to changes in both ECF volume and tonicity. The increase in tonicity plays a greater role in the elevation of pAVP, than the reduction in volume.

Animals↗
PubMed1982

Osmotic control of plasma vasopressin in the dog.

Seven dogs prepared with carotid loops were used to evaluate the responsiveness of the cerebral osmoreceptors regulating plasma vasopressin concentration (pAVP). Intracarotid and intravenous infusions of hypo- and hypertonic solutions were used to alter cerebral plasma osmolality. Bilateral intracarotid infusion of hypertonic saline (0.90 mmol NaCl kg-1 . min-1 . artery-1) significantly elevated jugular vein plasma osmolality (pOsm) in the first minute (P less than 0.05). Systemic values, determined from saphenous vein samples, were increased after 6 min. After 4 min of infusion, systemic pAVP was significantly increased, attaining a constant level at 6 min. Subsequent experiments with infusions 6 min in duration demonstrated that hypertonic saline infused intracarotidly significantly increased pAVP in a dose-related fashion, whereas similar solutions administered intravenously did not alter pAVP. Hypotonic infusions (intravenous or intracarotid) did not change pAVP consistently. The lack of a depression in pAVP during hypotonic infusions is consistent with the argument that jugular pOsm must be elevated above a threshold to stimulate the release of vasopressin. Linear relationships were demonstrated for jugular pNa+ and pOsm to pAVP employing the threshold model. Cerebral osmoreceptors that regulate plasma vasopressin concentration respond linearly to increasing tonicity above a threshold stimulating the release of vasopressin.

Animals↗
PubMed1982

Effect of hypertonic intracarotid infusions on plasma vasopressin concentration.

The effect of short-term bilateral intracarotid infusions of hypertonic saline on plasma vasopressin concentration (pAVP) was evaluated in five dogs. Intracarotid infusion of saline at 90 mumol . kg-1 . min-1 . artery-1 significantly (P less than 0.05) increased jugular vein osmolality (pOsm) and sodium concentration (pNa+) within 2 min. Saphenous vein pOsm was not altered during the 6 min of infusion, whereas pNa+ was increased (P less than 0.05) from 0.8 +/- 0.1 to 2.3 +/- 0.3 pg/ml. Subsequent experiments using hypertonic saline infusions of 90 and 180 mumol . kg-1 . min-1 administered intracarotidly and intravenously for 6 min were performed. Intracarotid isotonic infusions and intravenous hypertonic infusions did not significantly alter pAVP. Hypertonic intracarotid saline increased jugular vein pOsm and pNa+ in a dose-related fashion, whereas saphenous vein pOsm and pNa+ were not significantly changed after 6 min of infusion. Plasma vasopressin, compared with the isotonic intracarotid infusion (1.5 +/- 0.3 pg/ml), was increased (P less than 0.05) after hypertonic saline to 3.2 +/- 0.6 and 4.8 +/- 0.2 pg/ml for the 90 and 180 mumol . kg-1 . min-1 infusions, respectively. The cerebral osmolality indicated by jugular vein pOsm was therefore increased in the absence of changes in systemic pOsm during intracarotid hypertonic infusions. The increase in pAVP in response to these changes in pOsm supports the presence of central osmoreceptors regulating vasopressin release in the area of distribution of the common carotid arteries.

Adrenocorticotropic Hormone↗
PubMed1982

Hemodynamic, hormonal, and drinking responses to reduced venous return in the dog.

The effect of an acute reduction in venous return, caused by reversible constriction of the thoracic vena cava, on drinking and secretion or arginine vasopressin (AVP) was examined in the dog. Plasma AVP levels rose immediately from a control level of 1.4 +/- 0.1 pg/ml (mean +/- SE) to a plateau ranging between 36 and 42 pg/ml during the first 30 min after constriction but declined to 12.6 +/- 4.2 pg/ml 2 h after constriction even though systemic arterial hypotension was maintained. Drinking occurred with a latency of 22 +/- 6 min and 13.2 +/- 1.8 ml H2O/kg was consumed during 2 h of vena caval constriction. Water intake was significantly correlated with the average reduction in blood pressure (r = 0.86; n = 8; P less than 0.01) but not with plasma renin activity. The role of angiotensin II (ANG II) in the drinking and secretion of AVP in response to decreased venous return was evaluated using the ANG II receptor blocker, saralasin, infused intravenously (iv) or intracerebroventricularly (icv). Intravenous, but not icv, infusion of saralasin during vena caval constriction reduced the ability of the dogs to maintain arterial blood pressure (P less than 0.05). However, neither iv nor icv saralasin significantly affected water intake or the rise in plasma AVP in response to vena caval constriction when compared to their respective controls. Taken together, these data show that angiotensin is important in the maintenance of systemic arterial blood pressure but is not essential for the rise in plasma AVP or drinking in response to an acute reduction in venous return. It is suggested that either arterial baroreceptors or "low-pressure" volume receptors or both mediate the drinking and AVP responses in the presence of central blockade of the effects of circulating angiotensin.

Animals↗
PubMed1982

Lesions of the subfornical organ block angiotensin-induced drinking in the dog.

The role of the subfornical organ (SFO) in drinking caused by cellular dehydration and angiotensin was examined in the dog. Drinking responses to intravenous administration of angiotensin and to hypertonic NaCl were compared before and after electrolytic ablation of the SFO. After destruction of the SFO, drinking in response to angiotensin was 0.5 +/- 0.3 ml/kg compared to 11.9 +/- 3.7 ml/kg prior to lesioning. Drinking in response to hypertonic NaCl was not affected by lesioning the SFO (12.6 +/- 6.6 ml/kg before vs. 13.4 +/- 5.4 ml/kg after the lesion). Lesions superior or lateral to the SFO did not affect drinking in response to either angiotensin or hypertonic NaCl. These data show that the SFO is essential for drinking in response to blood-borne angiotensin but not to the stimulus of cellular dehydration in the dog.

Angiotensin II↗
PubMed1982

Apparent dissociation of adrenocorticotropin and corticosteroid responses to 15 ml/kg hemorrhage in conscious dogs.

The blood pressure, heart rate, ACTH, corticosteroid, vasopressin, and renin responses to rapid 15 ml/kg hemorrhage were measured in six conscious healthy dogs with chronically maintained femoral arterial catheters. The hemorrhage decreased the mean arterial blood pressure slightly (P less than 0.001), increased the heart rate (P less than 0.001), and increased arterial plasma levels of ACTH (P less than 0.01), corticosteroids (P less than 0.001), vasopressin (P less than 0.001), and renin activity (P less than 0.001). Overall and in the individual experiments, there appeared to be little correspondence between the ACTH and corticosteroid responses. In none of the experiments was there a clear rise in ACTH above control levels before the first rise in corticosteroids. To ascertain that adrenal secretion of corticosteroids was increased during 15 ml/kg hypovolemia, changes in the clearance and distribution volume of cortisol were estimated by counting tritium extracted from plasma of five dogs infused with [1,2-3H] cortisol to steady state levels before and during hypovolemia. The stimulus caused a 30% reduction from steady state levels of dichloromethane-extractable tritium counts (P less than 0.001). Combined with the observed increase in plasma corticosteroid levels, these results show that the increase in adrenal secretion of corticosteroids after hemorrhage was underestimated by measurement of changes in peripheral plasma levels. The hypothesis that hemorrhage results in an increase in adrenal sensitivity to ACTH is tested in the following paper.

Adrenal Cortex Hormones↗
PubMed1982

Lesions of the organum vasculosum of the lamina terminalis (OVLT) attenuate osmotically-induced drinking and vasopressin secretion in the dog.

Drinking and secretion of arginine vasopressin (AVP) in response to intravenous infusion of hypertonic NaCl were studied in dogs before and after destruction of the OVLT. The functional relationship between plasma osmolality and plasma AVP was eliminated following destruction of the OVLT. Furthermore, osmotically-induced drinking was significantly reduced in dogs with OVLT lesions. These data are compatible with the hypothesis that the OVLT contains osmoreceptors in the dog.

Animals↗