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T G Coleman

Publications and source records attributed to T G Coleman.

At least 37 records · Page 2Linked to original sources
PubMed1982

Meaning of the cardiac output-blood volume relationship in essential hypertension.

This study interprets the cardiac output-blood volume relationship in essential hypertension. Previous reports indicated that the chronic volume-flow slope (i.e., the regression coefficient alpha, cardiac output = alpha blood volume + beta, obtained from steady-state volume and flow) and the transient volume-flow slope observed during a dextran infusion were both steeper in essential hypertensives than in normotensives. By applying the Guyton-Coleman circulatory model to essential hypertension, this reports demonstrates that: 1) several alterations of the circulatory system may theoretically change the steady state of volume and flow and generate a chronic volume-flow relationship. However, only alterations of the kidney function and of the autonomic nervous system may produce a volume-flow curve compatible with the available data. 2) As hypertension develops, vascular resistance and compliance have the greatest influence on the slope of the chronic volume-flow curve. 3) To account for the observed increase of this slope in the transition from normotension to essential hypertension, not only must resistance be increased but also compliance must be reduced in essential hypertension. The same conclusions are drawn from the study of the transient volume-flow relationship observed during the dextran infusion.

Blood Volume↗
PubMed1982

Measurement of renal artery pressure in the rat.

The objective of this study was to develop and document a simple technique for the direct measurement of renal artery pressure (RAP) in the rat. RAP was recorded in 13 Sprague-Dawley rats using a glass micropipette fitted to a low displacement pressure transducer. Average mean arterial pressure recorded from a femoral artery catheter was 107.2 +/- 3.2 mmHg compared with a RAP of 103.8 +/- 3.7 mmHg (P less than 0.05). To determine whether the measurement affected renal blood flow (RBF), RBF was determined using radiolabeled microspheres, both before and while recording left RAP. No differences existed between the initial left and right RBFs [7.3 +/- 0.4 %CO/gm (percent cardiac output per gram tissue) vs. 7.3 +/- 0.4 %CO/gm, P greater than 0.9]. The micropipette in the left renal artery did not alter left RBF (control, 7.3 +/- 0.4 %CO/gm vs. experimental, 7.6 +/- 0.4 %CO/gm; P greater than 0.2). Right RBF did not change between successive flow determinations (P greater than 0.5) indicating that a change in renal hemodynamics unrelated to the protocol did not occur. The techniques presented provide an accurate, simple method for the direct measurement of RAP in the rat.

Animals↗
PubMed1981

Baroreceptor reflex in the rat after converting enzyme inhibition or angiotensin receptor blockade.

1. One component of baroreflex responsiveness was quantitated in conscious rats using the heart rate response to a pressor injection of phenylephrine. 2. Endogenous angiotensin and its effectiveness were manipulated by sodium deprivation, converting enzyme inhibition and infusion of an angiotensin analogue. None of these manoeuvres changed the observed reflex responsiveness. 3. We conclude that endogenous angiotensin has no influence on the component of baroreceptor function that is described by the slope of the arterial pressure-heart rate relationship.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1981

Control of glomerular filtration rate by circulating angiotensin II.

Previous studies from our laboratory have provided evidence that the renin-angiotensin system plays an important role in controlling glomerular filtration rate (GFR) through an efferent arteriolar vasoconstrictor mechanism; however, the relative importance of circulating versus intrarenally formed angiotensin II (ANG II) in this control has not been determined. In the present study, the role of circulating ANG II in regulating GFR during reduced renal artery pressure (RAP) was examined in sodium-depleted dogs. After 90 min of infusion of the angiotensin-converting enzyme inhibitor SQ 14225, which presumably inhibited formation of both circulating and intrarenal ANG II, reduction of RAP to 81 +/- 2 mmHg resulted in marked decreases in GFR, filtration fraction (FF), and calculated efferent arteriolar resistance (RE), whereas renal blood flow (RBF) was maintained approximately 40% above initial control levels determined before SQ 14225 infusion. Replacement of circulating ANG II during SQ 14225 infusion, by intravenous infusion of ANG II at rates that decreased RBF to control levels, increased GFR, FF, and RE to levels not significantly different from control while RAP was maintained constant by aortic constriction. These observations suggest that circulating ANG II plays an important role in regulating RE and GFR during reductions in RAP. The importance of intrarenally formed ANG II in controlling GFR remains to be determined.

Angiotensin II↗
PubMed1980

Long-term regulation of arterial pressure, glomerular filtration and renal sodium reabsorption by angiotensin II in dogs.

1. This study was designed to quantify the role of angiotensin II in determining the chronic relationships between arterial pressure, renal haemodynamics and sodium excretion. 2. In six control dogs sodium balance was achieved during chronic increases in sodium intake from 5 to 495 mmol/day with small increases in arterial pressure (7mmHg), moderate increases in glomerular filtration rate (19%) and decreases in filtration fraction. Similar increases in sodium intake in dogs whose circulating levels of angiotensin II were fixed, due to a constant intravenous infusion of 4.85 pmol of angiotensin II min-1 kg-1, caused large increases in arterial pressure (42%), glomerular filtration rate (31%), filtration fraction and calculated renal sodium reabsorption above control. In six dogs whose angiotensin II formation was blocked by SQ 14 225, sodium balance at intakes of 5-80 mmol/day occurred at reduced arterial pressure, glomerular filtration rate, filtration fraction and sodium reabsorption although plasma aldosterone concentration was not substantially different from that in control dogs. At sodium intakes above 240 mmoL/day arterial pressure was not altered by SQ 14 225. 3. These data indicate that during chronic variations in sodium intake angiotensin II plays a major role, independently of changes in plasma aldosterone concentration, in allowing sodium balance without large fluctuations in glomerular filtration rate or arterial pressure. The mechanism whereby angiotensin II conserves sodium chronically is through increased sodium reabsorption, since steady-state sodium reabsorption was increased by angiotensin II and decreased by SQ 14 225.

Aldosterone↗
PubMed1980

Pseudohypertension in sinoaortic-denervated rats.

1. Mean arterial pressure was determined continuously over a 24-h period by computerized data collection in eight control and nine sinoaortic-denervated rats housed in standard-sized metabolic cages. In addition, direct and indirect pressure measurements were made while the rats were resting in a Lucite restrainer. 2. Pressure measurements made during restraint indicated that the baroreceptor-denervated rats were hypertensive: mean aortic pressure averaged 145 +/- 3.4 mmHg (mean +/- SEM) in denervated rats vs 119 +/- 2.8 mmHg in control rats (P < 0.001), and tail-cuff pressure averaged 156 +/- 5.4 mmHg compared with 121 +/- 2.7 mmHg in the control group (P < 0.001). 3. In contrast, continuous pressure monitoring showed the sinoaortic-denervated rats were normotensive (mean arterial pressure averaged 119 +/- 4.7 mmHg vs 119 +/- 3.1 mmHg in control rats). 4. Apparently arterial pressure is elevated during restraint in sinoaortic-denervated rats and pressure measurements made under these conditions give a false indication of hypertension.

Animals↗
PubMed1980

Arterial baroreflex control of heart rate in the conscious rat.

Angiotensin II, methoxamine and phenylephrine were evaluated in two tests of reflex responsiveness that involve arterial pressure increases (delta BP) and reflex bradycardia (delta HR). First, bolus injections produced comparable ratios (delta HR/delta BP, in beats . min-1 . mmHg-1) for the three agents: 1.69 +/- 0.31, 1.80 +/- 0.30, and 1.59 +/- 0.32, respectively (SE, n = 6). All three agents also had some undesirable direct chronotropic effects on the heart. Phenylephrine and methoxamine produced rapid and predictable pressure changes and were stable in solution. Blockade by atropine and propranolol was used to show that the bradycardia after bolus injection has an early component (1 s after pressure maximum) that is wholly parasympathetic. In the second test, 5-min infusions of the three agents produced comparable final delta HR/delta BP ratios: 2.0 +/- 0.3, 2.2 +/- 0.5, and 2.3 +/- 0.2 for angiotensin, methoxamine, and phenylephrine, respectively (n = 6). delta HR in this case had a predominant (estimated 67% of total) beta-adrenergic component. Therefore, rapid vagal control of heart rate in the conscious rat is temporary; it is replaced and strengthened in time by a more slowly developing beta-adrenergic component. Bolus injection and infusion of vasopressors can be conveniently used in combination to more fully quantitate heart rate responsiveness in conscious animals that have implanted arterial and venous catheters.

Angiotensin II↗
PubMed1980

Mathematical model of the fetal cardiovascular system: the uncontrolled case.

A mathematical model was developed to study and to interpret the results of different experiments undertaken in the field of fetal cardiovascular physiology. This model consists of a total of six peripheral blood compartments and a detailed description of the heart. The unique characteristics of the fetal circulation, particularly the ductus arteriosus, the foramen ovale, and the placenta are incorporated into this model. No control mechanisms are incorporated. The model was validated by simulating several previously described experiments. First, the performance of the individual ventricles was measured. The results indicate that, in the normal physiological situation, the right ventricle is working near the upper limits of its function while the left ventricle works below its limits. Second, the circulatory system was stressed by increasing the blood volume and the results show a shift from right to left in the relative contributions of each ventricle to the total cardiac output. Finally, effects of clamping the several blood vessels of the umbilical cord were studied.

Animals↗
PubMed1980

Blood pressure and renal function during chronic changes in sodium intake: role of angiotensin.

The present study was designed to quantitate the role of the renin-angiotensin system (RAS) in determining the chronic relationships between arterial pressure (AP), renal hemodynamics, and Na excretion. In six control dogs, Na balance was achieved during chronic step increases in Na intake from 5 to 500 meq/day with small increases in AP (<7 mmHg), moderate increases in GFR (19%), and decreases in filtration fraction (FF) and plasma renin activity. Similar increases in Na intake in six dogs with angiotensin II (AII) fixed, due to constant intravenous infusion of 5 ng . kg-1 . min-1 AII, caused large increases in AP (42%), GFR (31%) FF, and calculated renal Na reabsorption (TNa) above control. In six dogs with AII formation blocked with SQ 14,225, Na balance at intakes of 5-80 meq/day occurred at reduced AP, GFR, FF, and TNa, although plasma aldosterone concentration (PAC) was not substantially different from that in control dogs. At Na intakes above 240 meq/day, AP was not altered by SQ 14,225. These data indicate that during chronic changes in Na intake the RAS plays a major role, independent of changes in PAC, in allowing Na balance without large changes in GFR or AP. The mechanism whereby AII conserves Na chronically is through increased TNa, since steady-state TNa was increased by AII and decreased by SQ 14,225.

Angiotensin II↗
PubMed1980

The role of the renal effects of angiotensin II in hypertension.

The renin-angiotensin system is involved in many forms of clinical and experimental hypertension. Although angiotensin II has powerful vasoconstrictor properties, it is doubtful that any substance can produce sustained hypertension solely by increasing total peripheral resistance. Since the authors have demonstrated previously that alterations in the kidney's ability to excrete sodium can affect long-term arterial blood pressure regulation, they investigated angiotensin's effect on renal function in several experimental models. The results of these studies clearly demonstrate that angiotensin has a powerful direct antinatriuretic effect, the magnitude of which is sufficient to cause marked hypertension at angiotensin concentrations well within the pathophysiological range.

Angiotensin II↗
PubMed1979

Whole body response of the peripheral circulation following hemorrhage in the rat.

Changes in mean circulatory filling pressure (MCFP) after hemorrhage reflect the whole-body response of the peripheral circulation to restore the driving force for venous return. In this study, changes in MCFP were measured for 15 min following a rapid 8 ml/kg hemorrhage. Three groups of rats were studied: 1) conscious, untreated; 2) conscious, ganglion blocked; and 3) pentobarbital anesthetized. In all three groups, hemorrhage decreased MCFP approximately 2.6 mmHg immediately after hemorrhage. In the conscious untreated rat, MCFP recovered 1.3 mmHg in 15 min; 83% of this recovery was complete within 2 min, and over 50% was complete by 30 s posthemorrhage. With ganglionic blockade, recovery was slowed to about 70% of that in the conscious, untreated animal during the first 5 min after hemorrhage. MCFP recovery was substantially depressed by pentobarbital, averaging only 42% of that in the untreated animal 5 min after hemorrhage. The results demonstrate that peripheral changes can quickly restore nearly 50% of the MCFP decrease occurring immediately after mild hemorrhage and that about one-third of this response is mediated by the sympathetic nervous system. Pentobarbital anesthesia greatly inhibits recovery, although its repressive mechanism is not known.

Animals↗
PubMed1979

Hypertension in dogs during antidiuretic hormone and hypotonic saline infusion.

Experimental hypertension was produced in 7 dogs by continuously infusing suppressor amounts of antidiuretic hormone (ADH) and hypotonic saline after renal mass had been surgically reduced to 30% of normal. Data were collected during 9 days of control measurements, 14 days of ADH and saline infusion, and then 3 days of saline infusion to 1) determine the chronic effects of ADH on arterial pressure and 2) determine whether hypertension could be maintained during hyponatremia. During the period of ADH infusion, arterial pressure increased to hypertensive levels while plasma sodium concentration decreased almost 20 meq/1. Also, during the ADH infusion period, the dogs demonstrated decreases in heart rate, plasm potassium concentration, plasma renin activity, and plasma aldosterone concentration. Fluid volume expansion was evidenced by sustained increases in blood volume and sodium space. We conclude that when renal function is compromised, subpressor amounts of ADH can contribute to the development of hypertension, probably due to its fluid-retaining properties and in spite of the attendant hyponatremia.

Animals↗