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J W DeClue

Publications and source records attributed to J W DeClue.

12 recordsLinked to original sources
PubMed1978

Arterial pressure-urinary output relationship in hypertensive rats.

The steady-state relationship between mean arterial pressure (AP) and output of sodium and water was determined for one-kidney control (1KC), one-kidney Goldblatt (1KG), normotensive Wistar-Kyoto (WKY), and Okamoto spontaneously hypertensive rats (SHR). Control fluid intake (given by intravenous infusion) was set at approximately 30 ml/day Ringer solution. The infusion rate was then increased progressively to 2, 4, and 8 times control for 24- to 48-h periods each. Control AP averaged 115 Torr in 1KC, 152 Torr in 1KG, 120 Torr in WKY, and 158 Torr in SHR. The eightfold increase in salt and water intake was accompanied by almost equal increase in salt and water output and increases in AP to 157 Torr in 1KC, 190 Torr in 1KG, 126 Torr in WKY, and 166 Torr in SHR. The arterial pressure-urinary output relationship in 1KG is parallel to that of 1KC but shifted to higher AP levels. Similarly, this relationship in SHR is parallel to that of WKY but shifted to higher AP levels. This parallel shift is indicative of uniform renal vasoconstriction but normal functional renal mass in the SHR.

Animals↗
PubMed1978

Subpressor angiotensin infusion, renal sodium handling, and salt-induced hypertension in the dog.

We studied the combined effect of subpressor amounts of angiotensin and long-term sodium chloride infusion on arterial pressure in 16 dogs for periods of 2--8 weeks. In dogs receiving 3.5 liters of isotonic NaCl daily, but no angiotensin, the arterial pressure increased an average of only 3 mm Hg. When angiotensin was infused continuously at a rate of 5 ng/kg per min (a rate too small to cause an observable immediate increase in pressure, subsequent infusion of 3.5 liters of saline daily then increased the pressure by 39 mm Hg. The urinary output of sodium increased to the same extent in both instances, that is, there was no extra sodium loss because of the elevated pressure. This suggests that the angiotensin significantly blocked the normal "pressure natriuresis" usually seen with such large increases in pressure. However, the plasma aldosterone levels during angiotensin infusion were not found to be different from those in the absence of angiotensin. Therefore, we have suggested that the tendency of the kidneys to retain sodium under the influence of angiotensin was probably caused mainly by a direct effect of angiotensin on the kidney itself. Such a direct renal sodium-retaining effect also could be a contributing factor in the marked hypertension that results from salt administration in the presence of small amounts of angiotensin.

Aldosterone↗
PubMed1976

Quantification of baroreceptor influence on arterial pressure changes seen in primary angiotension-induced hypertension in dogs.

We studied the role of the sino-aortic baroreceptors in the gradual development of hypertension induced by prolonged administration of small amounts of angiotensin II (A II) in intact dogs and dogs with denervated sino-aortic baroreceptors. Short-term 1-hour infusions of A II(1.0-100 ng/kg per min) showed that conscious denervated dogs had twice the pressor sensitivity of intact dogs. Long-term infusions of A II at 5.0 ng/kg per min (2-3 weeks) with continuous 24-hour recordings of arterial pressure showed that intact dogs required 28 hours to reach the same level of pressure attained by denervated dogs during the 1st hour of infusion. At the 28th hour the pressure in both groups was 70% of the maximum value attained by the 7th day of infusion. Both intact and denervated dogs reached nearly the same plateau level of pressure, the magnitude being directly related both the the A II infusion rate and the daily sodium intake. Cardiac output in intact dogs initially decreased after the onset of A II infusion, but by the 5th day of infusion it was 38% above control, whereas blood volume was unchanged. Heart rate returned to normal after a reduction during the 1st day of infusion in intact dogs. Plasma renin activity could not be detected after 24 hours of A II infusion in either intact or denervated dogs. The data indicate that about 35% of the hypertensive effect of A II results from its acute pressor action, and an additional 35% of the gradual increase in arterial pressure is in large measure a result of baroreceptor resetting. We conclude that the final 30% increase in pressure seems to result from increased cardiac output, the cause of which may be decreased vascular compliance. since the blood volume remains unaltered.

Angiotensin II↗
PubMed1976

Integration and control of circulatory function.

In this chapter we have emphasized especially the intrinsic controls of the circulation, such as the autoregulation mechanism for control of local blood flow, automatic control of cardiac output, long-term control of arterial pressure, long-term control of blood volume, and automatic distribution of fluids between the circulation and the interstitial spaces. The reasons for emphasizing these mechanisms are several: first, many experiments have now shown that the intrinsic mechanisms can provide highly stable long-term control of the circulation. Second, the value of the nervous and hormonal controls have probably been greatly overemphasized in the past. And, third, there are special complexities of the intrinsic controls--such as nonlinearities, delay in responses, and other effects--that have made these difficult to understand; it is probably these difficulties that have led to their underemphasis. However, we have not meant to take from the nervous and hormonal systems their true importance in circulatory control. For instance, intrinsic mechanisms have almost no capability for acute arterial pressure control (only for long-term control), and they have no mechanism for providing the drive necessary to make the animal ingest water and electrolytes. These require the nervous controls. Also, nervous reflexes are important in enhancing the effectiveness of blood volume control and control of cardiac pumping. Among the hormonal mechanisms, the renin-angiotensin system can provide a modest degree of arterial pressure control when the pressure falls below normal by eliciting a vasoconstrictor response in the peripheral blood vessels. However, this system seems to have an even more important renal function, a direct effect on kidneys to cause fluid retention; this in turn increases the body fluid volume and in this way increases the arterial pressure. Finally, the roles of ADH and aldosterone in the control of blood volume have probably been greatly overemphasized. On the other hand, both clinical experience and experimental studies are beginning to demonstrate that the thirst/ADH system is probably by far the most potent mechanism that we have for control of extracellular fluid sodium ion concentration. On the other hand, the aldosterone mechanism seems to be our primary control system for maintaining a normal extracellular fluid concentration of potassium.

Angiotensin II↗
PubMed1975

Fluid balance, renal function, and blood pressure.

After many detours in the search for the basic mechanism of hypertension, evidence now seems to corroborate the earliest concept that developed in the 1800's, namely, that hypertension almost always results from a tendency of the kidneys to retain water and salt. Animal studies show that the amount of excess body water and salt required to cause hypertension is exceedingly small, and that the hypertensive effect of the excess water and salt may not develop for days or weeks. When vascular constriciton occurs simultaneously, as occurs in the presence of large quantities of angiotensin, the blood volume may be less than normal, but even in these circumstances the fluid volume is relatively increased and is responsible for the hypertension because the vascular constrictont has decreased the capacity of the circulation to a greater extent than the decrease in blood volume.

Angiotensin II↗
PubMedDate not supplied

The role of the kidney in essential hypertension.

1. Many forms of human and experimental hypertension begin with compromised renal function. Essential hypertension may be another such case. 2. The kidneys of subjects with essential hypertension excrete normal amounts of salt and water at higher-than-normal renal perfusing pressures. Other overt signs of renal dysfunction are few; renal disease is excluded by definition. However, renal blood flow and glomerular filtration rate are usually less than normal in essential hypertension. 3. Renal afferent resistance can be calculated from arterial pressure, renal blood flow, and an estimate of glomerular capillary pressure. These calculations indicate that afferent resistance is increased to two or more times normal in essential hypertension. 4. It is not clear whether afferent constriction causes hypertension or results from it. The ability of high pressure to produce vascular damage points to the latter. But, most essential hypertensives show low-to-normal plasma renin levels and a marked afferent dilation after saline loading. These observations do not suggest nephrosclerosis: they are consistent with a causal role for afferent constriction. 5. We can speculate that, in essential hypertension, there is a defect in one of the mechanisms that sets afferent resistance. Afferent constriction could result from extrinsic influences (neural or humoral) or something totally within the kidney, such as abnormal handling of information from the macula densa. 6. The effect of afferent constriction on salt-and-water excretion would theoretically be offset by elevated arterial pressure so that the actual salt-and-water excretion would be normal, but only so long as the arterial pressure remained elevated.

Animals↗