Search PubMed⌕ Search

Biomedical subjects

T E Lohmeier

Publications and source records attributed to T E Lohmeier.

At least 37 records · Page 2Linked to original sources
PubMed1990

Chronic effects of a physiological dose of ANP on arterial pressure and renin release.

To determine the long-term effects of a physiological dose of atrial natriuretic peptide (ANP) on renin release, the renin response to reductions in renal arterial pressure (RAP) was studied during 1) control conditions and 2) acute and 3) chronic (5 days) intravenous infusion (5 ng.kg-1.min-1) of alpha-human ANP in conscious dogs maintained on a normal sodium intake. Renal perfusion pressure was servo controlled at reduced levels with an inflatable occluder placed around the abdominal aorta just above the renal arteries. Under control conditions, reducing RAP by 30 and 40 mmHg increased plasma renin activity (PRA) 4- to 5- and 9- to 10-fold, respectively. Acute ANP infusion had no significant effect on either basal levels of PRA or the PRA response to reduced RAP. During chronic ANP infusion there was a two- to threefold increment in plasma ANP concentration and approximately a twofold increase in urinary sodium excretion on day 1; however, there were no significant long-term changes in mean arterial pressure, basal PRA, or the levels of PRA achieved during reductions in RAP. These findings indicate that the changes in plasma ANP concentration that occur under normal physiological conditions do not appreciably alter either basal PRA or renin release in response to renal hypotension in conscious sodium-replete dogs studied under resting conditions.

Animals↗
PubMed1989

Sustained increases in plasma epinephrine concentration do not modulate renin release.

We examined the relationship between plasma renin activity (PRA) and renal arterial pressure (RAP) during 1) control conditions, 2) acute, and 3) chronic intravenous epinephrine (EPI) infusion (125 ng.kg-1.min-1). In eight conscious uninephrectomized dogs maintained on a normal sodium intake, the renin stimulus-response curve (RSRC) was determined by a stepwise reduction in RAP with an inflatable occluder around the renal artery controlled by a servo unit. The RSRC could be approximated by two lines intersecting at a threshold pressure (approximately 20 mmHg below control RAP). In the high-pressure range, PRA was relatively insensitive to changes in RAP, whereas, below threshold pressure, changes in RAP had large effects on PRA. During acute EPI infusion there was approximately a 40% increase in heart rate (control = 57 +/- 3 beats/min) and hematocrit (control = 30 +/- 1%) in association with a rise in plasma EPI concentration from 73 +/- 16 to 1,413 +/- 100 pg/ml; mean arterial pressure (MAP) was unchanged (94 +/- 3 mmHg). Moreover, EPI acutely increased basal PRA from 0.3 +/- 0.1 to 0.8 +/- 0.3 ng angiotensin I.ml-1.h-1 and shifted the RSRC to the right (increasing threshold pressure 7 mmHg) without altering the slope of the RSRC curve either above or below threshold pressure. In contrast, although plasma EPI concentration and hematocrit remained elevated during chronic EPI infusion, heart rate and basal PRA returned to preinfusion values. In addition, there were no significant long-term changes in MAP or in any of the parameters of the RSRC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Chronic hypotensive effects of verapamil in angiotensin hypertension are steroid independent.

This study was designed to examine the mechanisms that contribute to the chronic hypotensive effects of verapamil during angiotensin II-induced hypertension. Hypertension was induced in five dogs by continuous intravenous infusion of angiotensin II (5 ng/kg/min) for 17 days. On the sixth day of angiotensin II infusion when daily sodium balance was achieved, mean arterial pressure (control, 92 +/- 4 mm Hg), plasma aldosterone concentration (control, 5.2 +/- 0.9 ng/dl), and renal resistance (control, 0.28 +/- 0.01 mm Hg/ml/min) were increased 37 +/- 8 mm Hg, 13.6 +/- 5.0 ng/dl, and 0.20 +/- 0.05 mm Hg/ml/min, respectively. At this time there were no significant changes in glomerular filtration rate, effective renal plasma flow, net sodium and water balance, or extracellular fluid volume. Subsequently, when verapamil was infused (at 2 micrograms/kg/min) simultaneously with angiotensin II (days 7-13), there was a net loss of 55 +/- 10 meq sodium, a 7.0 +/- 0.7% fall in extracellular fluid volume, and approximately a 70% reduction in the chronic effects of angiotensin II on mean arterial pressure and renal resistance; in contrast, verapamil failed to attenuate the long-term aldosterone response to angiotensin II. Further, although glomerular filtration rate and effective renal plasma flow tended to increase during verapamil administration, there were no consistent chronic long-term changes in these renal indexes. In comparison with these responses in hypertensive dogs, when verapamil was infused for 7 days before the induction of angiotensin II hypertension, there were no significant changes in any measurements except mean arterial pressure, which fell 11 +/- 1 mm Hg. Thus, these data fail to support the hypothesis that the chronic stimulatory actions of angiotensin II on aldosterone secretion are dependent on a sustained increase in transmembranal calcium influx. Moreover, these data indicate that the pronounced long-term hypotensive effects of verapamil in angiotensin II hypertension are due to impairment of the direct renal actions of angiotensin II rather than the indirect sodium-retaining effects that are mediated via aldosterone secretion.

Aldosterone↗
PubMed1988

Disparity between renal venous norepinephrine and renin responses to sodium depletion.

To evaluate the hypothesis that sodium depletion produces a chronic increase in renal nerve activity, arterial and renal venous plasma norepinephrine (NE) concentrations were measured in conscious dogs subjected to various degrees of sodium depletion. After 9 days of sodium depletion (LS), there was a net loss of 69 +/- 10 meq sodium, and mean arterial pressure (MAP) was reduced from 94 +/- 5 to 88 +/- 4 mmHg. At this time plasma renin activity (PRA) was increased from a control level (sodium intake = 45 meq/day) of 0.34 +/- 0.08 to 1.47 +/- 0.26 ng angiotensin I (ANG I).ml-1.h-1 in association with an approximately sixfold increase in the PRA gradient across the kidneys. Subsequently, when captopril was infused during an additional 7 days of sodium deprivation [(LS + converting enzyme inhibitor CEI)], there was further sodium depletion (31 +/- 11 meq) and hypotension (MAP = 65 +/- 6 mmHg) and PRA and the renal PRA gradient increased even further. In marked contrast, there were no significant changes in either arterial plasma NE concentration (control = 102 +/- 5 pg/ml) or the renal arteriovenous gradient of plasma NE concentration during either LS or LS + CEI. These experiments show a distinct disparity between changes in the PRA and the plasma NE concentration gradient across the kidneys during LS and fail to support the contention that increased renal nerve activity is an important long-term adaptive response to sodium depletion.

Animals↗
PubMed1986

Cardiovascular and renal responses to chronic vasopressin infusion.

Arginine vasopressin (AVP) was infused into the renal artery of seven uninephrectomized conscious dogs at successive rates of 0.09, 0.36, and 1.46 ng X kg-1 X min-1 for 18, 9, and 5 days, respectively; subsequently, the nonpressor analogue of AVP, 1-desamino-8-D-arginine vasopressin (DDAVP), was infused intrarenally for 7 additional days. The lowest infusion rate of AVP produced a high concentration of AVP in the renal circulation (maximal antidiuresis) with only a relatively moderate increase in peripheral plasma AVP concentration. For comparison, the effects of a comparable increase in peripheral plasma AVP concentration during intravenous infusion at this same rate were observed in an additional group of dogs. Acutely, when this low dose of AVP was infused either intrarenally or intravenously, there was marked antidiuresis, but there were no significant changes in mean arterial pressure (MAP), renal hemodynamics, or urinary electrolyte excretion. Chronically, in both groups of animals, cumulative water balance was positive, and glomerular filtration rate, effective renal plasma flow, and MAP (16-18 mmHg) all increased; plasma renin activity decreased. Similar changes were observed during DDAVP infusion. When elevated peripheral plasma levels of AVP were achieved during the higher infusion rates of AVP, natriuresis and diuresis occurred, but, otherwise there was little change in the above variables, including MAP. Thus the hydrosmotic effects of AVP appear to account for its moderate hypertensive activity. Further, the failure of AVP to produce prominent hypertension, even when pronounced systemic vasoconstrictor effects are manifested, may be a result of its inability to promote significant renal vasoconstriction and antinatriuresis.

Aldosterone↗
PubMed1986

Current concepts and perspectives of renal volume regulation in relationship to hypertension.

The renal-body fluid mechanism for arterial pressure control is almost certainly the most primitive of all the pressure-regulating mechanisms in animals. Through the stages of evolution, the system has been greatly improved. Nervous controls provide rapid pressure-control mechanisms that function almost instantaneously, many hours or days before the renal-body fluid mechanism can act fully. The renin-angiotensin-aldosterone system plays another important role: this system ensures that very large changes in salt intake, from as little as one-tenth normal up to as high as 10 times normal, have very little effect on the regulated level of the arterial pressure. Finally, the long-term autoregulatory mechanism helps to dissociate the long-term control of cardiac output from long-term control of arterial pressure; it also makes it possible for extremely slight increases in body fluid volume to cause chronic volume-loading hypertension.

Aldosterone↗
PubMed1981

Blood pressure regulation: basic concepts.

In this paper we have attempted to explain the difference between proportional pressure control systems and the renal-blood volume-pressure control mechanism, which is an infinite gain pressure control system. Because of this infinite gain of the kidney mechanism, this mechanism has the capability of returning arterial pressure all the way back to the control leve. Furthermore, this mechanism can override the other pressure control mechanisms because of its extreme control capability. On the other hand, the renal-blood volume mechanism for pressure control itself be controlled by many other factors. These other factors are said to change the pressure "set-point" level of the renal system, and then the renal system automatically brings the pressure to the set-point level. It is especially noteworthy, however, that some of the factors that play extreme roles in short-term pressure control-such as heart strength, vascular capacity, and total peripheral resistance-will not alter the long-term arterial pressure level (unless they in some way concurrently alter the set-point of the kidney mechanism).

Aldosterone↗
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↗
PubMed1978

The relationship between body fluid volume, sodium ion concentration, and sensitivity to pressor effect of angiotensin II in dogs.

Extracellular fluid volume, plasma electrolyes, and plasma angiotensin II (A II) were individually controlled to determine their influence on the acute pressor responsiveness to A II. Hemodialysis of nephrectomized dogs was used to simulate and control the changes of major variables which occur in the intact state during changes in sodium balance. A II dose-pressure response curves were determined in 11 dogs at three volume states with plasma [Na+] maintained constant and in five dogs at low, normal, and high plasma [Na+] with body fluid volume maintained constant. Parallel shifts of the log dose-response curves were obtained in the three volume states. The same rise in arterial pressure with identical doses of A II was obtained at normal, contracted, and expanded volume states, with the change of arterial pressure based on the uncompensated basal pressure level at each volume state. When the fall in pressure observed during volume depletion was returned to control levels with norepinephrine, there was no change in the A II dose-response relationship from the control state. No difference in the A II dose-pressure response relationship was obtained between states of 140, 146, and 156 mEq/liter plasma [Na+] with body fluid volume held constant. The studies indicate that short-term alterations in either sodium or water balance do not alter the "real" vascular sensitivity to A II. The "apparent" changes normally observed result from preexisting endogenous levels of circulating A II present at the time the dose-response curve is determined which probably alter the availability of receptor sites to A II.

Angiotensin II↗
PubMed1977

Intrarenal role of angiotensin II in controlling sodium excretion during dehydration in dogs.

1. The intrarenal role of angiotensin II in controlling sodium excretion was examined in anaesthetized, dehydrated dogs by infusing the angiotensin II antagonist Sar1-Ile8-angiotensin II directly into the renal artery. Comparisons were made with dehydrated dogs receiving only sodium chloride solution intrarenally. 2. Intrarenal angiotensin II blockade resulted in significant increases in urinary sodium excretion and urine flow rate. 3. The results indicate that during the high-renin state of dehydration endogenous angiotensin II has intrarenal effects which lead to salt and water retention.

Angiotensin II↗
PubMed1977

[Des-Asp1] angiotensin II: mediator of the renin-angiotensin system?

Angiotensin II and its C-terminal heptapeptide fragment, [des-Asp1]angiotensin II, influence a variety of angiotensin receptors in a qualitatively similar manner. On the basis of potency studies, angiotensin II appears to be the important mediator of the renin-angiotensin system at the peripheral arteriolar receptors to maintain arterial blood pressure. However, both angiotensin II and the heptapeptide are approximately equally potent at receptor sites in the adrenal cortex, the renal arterioles, and the juxtaglomerular cells of the kidneys. Adrenal cortical receptor affinity appears to be greater for the heptapeptide than for angiotensin II. Analogues of the heptapeptide are better antagonists than analogues of the octapeptide in blocking the steroidogenic responses to both angiotensin II and heptapeptide. Circulating plasma levels of [des-Asp1]angiotensin II appear to be low in most species; there is strong evidence, however, that local generation of heptapeptide can occur under certain conditions. It seems likely that both peptides act at common receptor sites to mediate the response to the renin-angiotensin system but more data are needed before a definite physiologic role can be assigned to the heptapeptide.

Adrenal Cortex↗