Role of blood pressure in the control of renin release.
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Animals↗
Biomedical subjects
H Ehmke
Publications and source records attributed to H Ehmke.
Sympathetic modulation of renal hemodynamics, renin release and sodium excretion.
In anesthetized animals it has been shown previously, that the influence of electrical stimulation of efferent renal nerves on renal function with increasing stimulation frequencies can be graded; renin release is affected at low, sodium excretion at intermediate and vascular resistance at high stimulation frequencies. Experiments in conscious dogs are reviewed, which present evidence for a similar functional dissociation under physiological conditions. Moderate activations of the renal sympathetic nerves, which do not change renal blood flow 1) decrease sodium excretion independent of changes in angiotensin II, 2) interact with the pressure-dependent mechanism of renin release by resetting its threshold pressure and 3) modulate autoregulation by increasing the lower limits of glomerular filtration rate and renal blood flow-autoregulation. These findings may contribute to our understanding of the role of the renal nerves in the pathophysiology of congestive heart failure and hypertension.
Animals↗
Resetting of pressure-dependent renin release by intrarenal alpha 1-adrenoceptors in conscious dogs.
We investigated the influence of a stimulation of intrarenal alpha 1-adrenoceptors on the relationship between renin release and renal artery pressure in 8 conscious, chronically instrumented dogs receiving a normal salt diet. Renin stimulus-response curves were determined by a stepwise reduction of renal artery pressure down to 70 mm Hg (1) under control conditions, (2) during a bilateral common carotid occlusion combined with an intrarenal prazosin infusion, and (3) during an intrarenal methoxamine infusion. Both drug infusions did not alter resting renal blood flow. (1) The control renin stimulus-response curve revealed a flat portion (plateau-level) around and above the resting blood pressure and a very steep portion (slope) below a well-defined threshold pressure 10-15 mm Hg below the resting blood pressure. (2) An intrarenal alpha 1-adrenoceptor blockade by prazosin prevented the resetting of the threshold pressure which is regularly observed during bilateral common carotid occlusion. (3) An intrarenal infusion of the alpha 1-adrenoceptor agonist methoxamine increased the threshold pressure. We suggest that the neural control of renin release within the autoregulatory range of renal blood flow involves two independent mechanisms: the direct release of renin from juxtaglomerular granular cells by beta 1-adrenoceptors, and the modulation of the threshold pressure of pressure-dependent renin release by intrarenal alpha 1-adrenoceptors. The small changes in renal nerve activity necessary to reset the threshold pressure and the close relationship between the threshold pressure and resting blood pressure imply an important function of intrarenal alpha 1-adrenoceptors in the regulation of renin release.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
ANP and sodium excretion during acute baroreflex hypertension in conscious dogs.
The influence of an acute baroreflex hypertension elicited by common carotid occlusion (CCO) on plasma atrial natriuretic peptide (ANP) and renal sodium excretion was investigated in chronically instrumented, conscious foxhounds receiving a normal-sodium diet. CCO (n = 6) significantly increased mean arterial pressure (from 102 +/- 5 to 144 +/- 3 mmHg; P less than 0.01) and sodium excretion (from 82 +/- 10 to 133 +/- 9 mumol/min; P less than 0.05). No changes in plasma ANP and right atrial pressure were observed during the acute hypertension. In contrast, an acute 20% volume expansion (n = 7) corresponding to 1.8% of body weight raised right atrial pressure (from 1.3 +/- 1.2 to 5.8 +/- 1.2 cmH2O; P less than 0.01) and induced a sustained elevation of plasma ANP (from 39 +/- 8 to 67 +/- 16 pg/ml; P less than 0.05). The natriuresis in response to CCO was eliminated when renal perfusion pressure was regulated at the control level by a renal arterial cuff (n = 4); under these conditions, sodium excretion even tended to decrease during CCO (from 81 +/- 17 to 46 +/- 13 mumol/min; P less than 0.05). In conclusion, an increase in renal perfusion pressure and not an elevated ANP level is important in mediating the natriuresis during CCO in conscious dogs. These results imply that changes in plasma ANP are not essential for the induction and maintenance of a pressure natriuresis.
Acute Disease↗
Modulation of natriuresis by sympathetic nerves and angiotensin II in conscious dogs.
The effects of renal perfusion pressure and reflex sympathetic nerve stimulation on sodium excretion were studied in six conscious foxhounds on a normal sodium diet. This was done before, during common carotid occlusion (CCO), and during a recovery period following CCO. Three protocols were used 1) control (n = 6), 2) converting-enzyme inhibition (CEI, n = 6), and 3) CEI combined with a constant renal artery pressure (RAP, n = 5). In protocol 1, CCO increased RAP markedly (140.5 +/- 5.1 vs. 103.0 +/- 4.4 mmHg; P less than 0.001) along with a considerable natriuresis (128.4 +/- 20.1 vs. 86.3 +/- 15.1 mumol Na+/min; P less than 0.05). In protocol 2, CEI increased control sodium excretion but did not impair the natriuresis by CCO. Maintaining RAP at control levels in protocol 3 lead to an antinatriuresis (53.1 +/- 16.8 vs. 128.3 +/- 32.2 mumol Na+/min; P less than 0.05). Creatinine clearance was unaffected by all procedures. In conclusion, a change in ANG II formation shifts but does not impair the natriuretic response to CCO. A moderate sympathetic activation has a pronounced pressure-independent antinatriuretic effect, which is not mediated by angiotensin II.
Angiotensin I↗
Role of the kidney in long-term control of blood pressure.
In the central nervous system the afferents signalling either volume in the low pressure system ("cardiopulmonary afferents") or pressure in the arterial system (arterial baroreceptors) interact in a sense of a nonadditive attenuation, and only a complete denervation of both groups of afferents induces a chronic hypertension. Pressure natriuresis seems to contribute significantly in avoiding excessive hypertension in many states of chronic sodium and water retention. The variables threshold pressure and slope of the "renal baroreceptor"--mechanism of renin release serve different physiological functions: changes in slope (sensitivity) counteract short term changes in sodium balance whereas threshold pressure ensures a minimal systemic blood pressure associated with normal glomerular filtration. Sympathetic "resetting" of threshold pressure may play a pathophysiological role in some forms of hypertension and in the sodium retention of early congestive heart failure.
Animals↗
Physiology of the renal baroreceptor mechanism of renin release and its role in congestive heart failure.
The function of the renal baroreceptor can be quantitatively described by a stimulus-response curve showing a flat section in the high pressure range, a steep slope in the low pressure range, and a well-defined threshold pressure slightly below resting systemic pressure. This stimulus-response curve shows a close functional relation to autoregulation of renal blood flow, glomerular filtration rate and sodium excretion. Threshold pressure and slope are subject to different physiologic control mechanisms: The slope is increased by a low sodium diet, whereas threshold pressure is elevated by an increased renal sympathetic nerve discharge or by circulating catecholamines. Sympathetic influences also reset renal autoregulation. Recent studies have provided evidence for an important role of the renal baroreceptor in the long-term control of arterial blood pressure. The sympathetic modulation of threshold pressure can induce sodium retention in early heart failure, and the sympathetic effects on autoregulation may help to explain clinical reports on a deterioration of renal function during converting-enzyme therapy.
Animals↗
Effect of sino-aortic denervation in comparison to cardiopulmonary deafferentiation on long-term blood pressure in conscious dogs.
The isolated and combined influence of cardiopulmonary and sinoaortic denervation on long-term blood pressure (MAP), heart rate (HR), plasma renin activity (PRA) and plasma volume (PV) was studied in 11 conscious, chronically instrumented foxhounds receiving a normal sodium diet. MAP, HR, PV and PRA remained unchanged in the 5 dogs after bilateral thoracic vagal stripping, which eliminates the cardiopulmonary afferents. After sino-aortic denervation in another 5 dogs there was equally little change when compared to the control group. Only total baroreceptor and cardiopulmonary denervation (7 dogs) revealed significantly higher levels of MAP (119.6 +/- 4.6 vs. 100.4 +/- 1.5, P less than 0.01), HR (118.2 +/- 3.7; vs. 84.1 +/- 3.5; P less than 0.0001), and PRA (3.6 +/- 0.9 vs. 0.9 +/- 0.2; P less than 0.05). In conclusion, the function of either arterial baroreceptors or cardiopulmonary receptors is sufficient for normal circulatory control. When both groups of receptor afferents are interrupted, MAP, HR, and PRA rise to significantly higher levels. Thus, both systems interact in a sense of a non-additive attenuation on "cardiovascular centres". This may clarify previous disputes concerning neurogenic hypertension, and supplies information for the role of the renin-angiotensin system in blood pressure control.
Afferent Pathways↗
Influence of the renin-angiotensin system on the autoregulation of renal blood flow and glomerular filtration rate in conscious dogs.
Renal autoregulation of blood flow (RBF) and glomerular filtration rate (GFR) were examined in 10 conscious foxhounds under a normal sodium diet before and after a continuous intrarenal converting-enzyme inhibition (CEI) or during the application of the angiotensin II antagonist saralasin. In order to prevent alpha-adrenergic interference, phenoxybenzamine was infused into the renal artery. In contrast to studies performed in salt depleted dogs there was no impairment of RBF or GFR autoregulation after CEI or saralasin. Renal blood flow was autoregulated at a level of 3.81 +/- 0.18 ml min-1 g-1 in the control group, 3.98 +/- 0.16 ml min-1 g-1 after CEI and 3.97 +/- 0.41 ml min-1 g-1 after saralasin. The lowest point of autoregulation was very much the same between the individual groups (control: 65.0 +/- 1.4 mmHg; CEI: 66.5 +/- 4.6 mmHg; saralasin: 67.4 +/- 3.2 mm Hg). GFR acted in a similar manner (autoregulation level control: 0.50 +/- 0.03 ml min-1 g-1; CEI: 0.52 +/- 0.05 ml min-1 g-1; saralasin. 0.50 +/- 0.04 ml min-1 g-1). The lowest pressure of GFR autoregulation differed slightly more (control: 81.5 +/- 2.2 mmHg; CEI: 93.2 +/- 4.2 mmHg; saralasin: 85.9 +/- 2.1 mmHg). The results suggest that the renal autoregulation of GFR and RBF is independent of the renin-angiotensin system in conscious dogs during a normal sodium diet.
Angiotensin-Converting Enzyme Inhibitors↗
Autoregulation of renal blood flow, glomerular filtration rate and renin release in conscious dogs.
The relationship between renal artery pressure (RAP), renal blood flow (RBF), glomerular filtration rate (GFR) and the renal venous-arterial plasma renin activity difference (PRAD) was studied in 22 chronically instrumented, conscious foxhounds with a daily sodium intake of 6.6 mmol/kg. RAP was reduced in steps and maintained constant for 5 min using an inflatable renal artery cuff and a pressure control system. Between 160 and 81 mm Hg we observed a concomitant autoregulation of GFR and RBF with a high precision. The "break off points" for GRF- and RBF-autoregulation were sharp and were significantly different from each other (GFR: 80.5 +/- 3.5 mm Hg; RBF: 65.6 +/- 1.3 mm Hg; P less than 0.01). In the subautoregulatory range GFR and RBF decreased in a linerar fashion and ceased at 40 and 19 mm Hg, respectively. Between 160 mm Hg and 95 mm Hg (threshold pressure for renin release) PRAD remained unchanged; below threshold pressure PRAD increased steeply (average slope: 0.34 ng AI.ml-1.h-1.mm Hg-1) indicating that resting renin release may be doubled by a fall of RAP by only 3 mm Hg. At the "break-off point" of RBF-autoregulation (66 mm Hg) renin release was 10-fold higher than the resting level. It is concluded that under physiological conditions (normal sodium diet) GFR and RBF are perfectly autoregulated over a wide pressure range. Renin release remains suppressed until RAP falls below a well defined threshold pressure slightly below the animal's resting systemic pressure. RBF is maintained at significantly lower pressures than GFR, indicating that autoregulation of RBF also involves postglomerular vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A physiological role for pressure-dependent renin release in long-term blood pressure control.
The relationship between pressure-dependent renin release and long-term blood pressure was studied in 14 conscious dogs on a normal salt diet. Stimulus-response curves were obtained by a controlled reduction of renal artery pressure in 5 or 10 mm Hg steps down to 70 mm Hg. Pressure-dependent renin release was characterized by a threshold pressure, a plateau above threshold pressure, and a steep slope below the threshold pressure. In each dog long-term blood pressure was higher than threshold pressure. Threshold pressure and slope were found to describe more than 90% of long-term blood pressure variability between conscious dogs. The following findings suggest that an on-off switch of pressure-dependent renin release stabilizes long-term blood pressure above the threshold pressure: (1) The intermittent activation of pressure-dependent renin release due to physiological variations in arterial blood pressure induced changes in plasma renin activity by as much as 300%. (2) The individual difference between threshold pressure and long-term blood pressure was highly dependent on the slope. (3) A systemic blockade of the renin-angiotensin system by converting-enzyme inhibition resulted in a slope-dependent fall of long-term blood pressure. (4) A spontaneous shift of threshold pressure was accompanied by equivalent changes in arterial blood pressure. Taken together, our results provide evidence for a major role of pressure-dependent renin release in the long-term control of blood pressure in conscious dogs. A chronic resetting of threshold pressure may be an important mechanism in the pathogenesis of hypertension.
Animals↗
[The menstrual cycle after hormonal growth inhibition in girls].
Up to 1979 growth was inhibited with hormones in 43 girls in puberty with constitutional gigantism. The average reduction in size as compared to the calculated final body height was 7.5 cm, treatment having been started at a skeletal age of 12.3 years and with a treatment duration of 1.4 years. In over 90% of the cases, the first spontaneous menstruation after termination of therapy occurred within three months. During the first two years, cycles were likewise regular in 90% of the cases, with a duration of 4 +/- 1 weeks. Ovarian function in adolescence was thus found not to be impaired, but rather to be more stable as compared to the total population. It may be concluded from this that the preconditions for future fertility can be regarded as favorable.
Adolescent↗
[Choledochal diverticulum as a possible cause of right-sided upper abdominal pain].
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Abdomen↗
The influence of cardiopulmonary receptors on long-term blood pressure control and plasma renin activity in conscious dogs.
The isolated and combined influence of cardiopulmonary and arterial baroreceptor denervation on long-term blood pressure (MAP), heart rate (HR), plasma volume (PV) and plasma renin activity (PRA) was studied in 10 conscious, chronically instrumented foxhounds receiving a normal sodium diet. Cardiopulmonary denervation was achieved by surgically stripping both thoracic vagi. Near complete arterial baroreceptor denervation, leaving most cardiopulmonary fibres intact, was made by left vagal deafferentiation which has been shown to eliminate most aortic baroreceptor afferents, and a carotid sinus denervation. Five groups were studied: (I) control (n = 9), (II) cardiopulmonary denervation (n = 5), (III) aortic baroreceptor denervation (n = 5), (IV) arterial baroreceptor denervation (n = 4) and (V) total denervation (n = 6). No changes in PV were observed. Only group V revealed significantly higher levels of MAP (119.5 +/- 5.4 vs. 100.1 +/- 1.6 mmHg; P less than 0.05), HR (118.1 +/- 4.4 vs. 87.8 +/- 3.7 beats min-1; P less than 0.001) and PRA (3.0 +/- 0.8 vs. 0.9 +/- 0.2 ng AI m-1 h-1; P less than 0.05). It is suggested that the isolated function of either cardiopulmonary or arterial baroreceptors is sufficient to maintain these variables at a normal level. Contrary to the results of other reports the cardiopulmonary receptors do not seem to regulate MAP at a level about which the arterial baroreceptors operate. When both groups of afferents were interrupted MAP, HR and PRA rose to significantly higher levels, implying that cardiopulmonary and arterial baroreceptor afferents interact in a sense of a non-additive attenuation.
Animals↗
Sympathetic modulation of the pressure-dependent renin release in conscious dogs.
The relationship between mean renal artery pressure and renal venous-arterial plasma renin activity-difference (renin stimulus-response curve; RSRC) was studied in 15 conscious dogs by a stepwise reduction of renal artery pressure down to the lower limit of renal blood flow (RBF)-autoregulation. The RSRC has a flat section above threshold and a steep slope - indicating a 100% increase of renin release per 2.5 mmHg - below a well defined threshold pressure (Pth). Pth may remain unchanged for 4 weeks. A reflex activation of the renal sympathetic nerves by common carotid occlusion increased Pth by 16.5 +/- 3.2 mmHg (P less than 0.01); this effect was abolished by intrarenal alpha-blockade (prazosin). A low dose intrarenal infusion of methoxamine, which did not change RBF, increased Pth by 8.5 +/- 0.7 mmHg (P less than 0.001). We conclude that in the resting conscious dog renal perfusion pressure is a powerful factor in the control of renin release. The renal sympathetic nerves modulate the pressure-dependent mechanism within the autoregulatory range of renal blood flow by an alpha-adrenergic adjustment of threshold pressure.
Animals↗
Pressure-dependent renin release: the kidney factor in long-term control of arterial blood pressure in conscious dogs.
In 12 conscious dogs on a normal sodium diet the renal venous-arterial plasma renin activity-difference as a function of mean renal artery pressure (renin stimulus-response curve; RSRC) as well as long-term mean arterial blood pressure (MAP; pressure-histograms) were measured repeatedly. The RSRC has 1) a threshold pressure (Pth), 2) a flat section above Pth (plateau-level), and 3) a steep slope below Pth. From dog to dog the slope varied from -0.20 to -0.54 ng AI/ml/h/mmHg and Pth from 78.4 to 107.1 mmHg. In every dog MAP was higher than Pth (MAP-Pth:12.8 +/- 1.58 mmHg). Dogs with a higher Pth regularly showed a higher MAP (r = 0.76; P less than 0.005). Due to its normal variability arterial pressure occasionally falls below Pth and thus causes renin release. Therefore MAP will stabilize at a level above Pth. The pressor effect (MAP-Pth) of this feedback system should depend on the sensitivity of the pressure-dependent renin release mechanism (slope of RSRC). Accordingly we observed a close correlation between the slope of the RSRC and the MAP-Pth difference (r = 0.93; P less than 0.0001). We conclude that in healthy dogs the level of long-term blood pressure can be explained almost completely by Pth and the slope of the pressure-dependent renin release. Our findings may offer new perspectives to the pathogenesis of hypertension.
Animals↗