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H Ehmke

Publications and source records attributed to H Ehmke.

At least 55 records · Page 3Linked to original sources
PubMed1995

Frequency domain of renal autoregulation in the conscious dog.

The dynamic range in which renal blood flow (RBF) autoregulation occurs was determined in eight conscious foxhounds chronically catheterized in the abdominal aorta and implanted with a transit-time flow probe over the renal artery. Sinusoidal driving pressures (amplitude of 10 mmHg) were forced on the renal arterial pressure at different frequencies by a servo-control device, and transfer functions were calculated. Only one frequency range was found below which the gain of the transfer function declined and in which the phase angle increased (n = 8). This indicates the presence of a potent mechanism for renal autoregulation in the examined frequency range between 0.0031 and 0.08 Hz, which buffers changes in blood flow < 0.02 Hz. After furosemide treatment, one indicator for autoregulation (phase shift of transfer function) was significantly blunted at low frequencies (n = 6). Furosemide, however, did not reduce the phase shift to zero, suggesting that some autoregulation still remained in the frequency range between 0.04 and 0.08 Hz. In conclusion, autoregulation of RBF during sinusoidal changes in driving pressure between 0.0031 and 0.02 Hz is mediated by a single mechanism, which can be blocked by the acute administration of furosemide. The residual phase shift between arterial pressure and RBF in the transfer function observed during sinusoidal changes in driving pressure between 0.04 and 0.08 Hz suggests the presence of a second mechanism for RBF autoregulation.

Animals↗
PubMed1995

Nitric oxide synthase and vasoactive intestinal polypeptide colocalization in neurons innervating the human penile circulation.

The question which neurotransmitters mediate penile erection in humans is still unsettled. Although functional studies have established a role of vasoactive intestinal polypeptide (VIP) and nitric oxide (NO) in human penile smooth muscle relaxation, they did not allow a conclusion as to whether they are released by neurons or other cells. This article outlines the identification of numerous nitric oxide synthase (NOS) and VIP-containing axons in the human penis. More than 50% of the perivascular nerve fibres and more than 90% of the trabecular nerve fibres within the corpus cavernosum stained positive for both NOS and VIP. In contrast, endothelial cells stained only faintly for NOS-immunoreactivity, NOS/VIP-immunoreactivity was reduced (diabetes) or absent (lesion of the cavernous nerve) in penile tissue taken from patients with neurogenic impotence. These findings support the concept that NO and VIP act as neural comediators of penile erection in humans.

Humans↗
PubMed1994

The blood pressure buffering capacity of nitric oxide by comparison to the baroreceptor reflex.

To compare the contribution of nitric oxide (NO) to the buffering of short-term and circadian fluctuations of arterial blood pressure with that of the baroreceptor reflex, conscious foxhounds were subjected to continuous 24-h blood pressure recordings. A pressure transducer was placed into the lumen of the abdominal aorta. Telemetry recordings were done under control conditions, following blockade of NO formation by intravenous bolus injection of NG-nitro-L-arginine (L-NNA; 16.5 +/- 2 mg/kg body wt) and after total sinoaortic and cardiopulmonary denervation in five dogs each. L-NNA produced a sustained elevation of mean arterial pressure (MAP; 137.2 +/- 6.4 mmHg vs. control, 112.9 +/- 3.7 mmHg). After denervation, no significant increase of MAP was found (113.5 +/- 4.1 mmHg), but the standard deviation of the MAP histogram was significantly greater (22.5 +/- 3.1 vs. 10.6 +/- 0.9 mmHg, P < 0.05). Sequential spectral analysis showed that total power between 0 and 0.5 Hz was elevated more than twofold after L-NNA (P < 0.05). This was due primarily to increased power in the range above 0.1 Hz. After denervation, total power increased about three-fold (P < 0.05), almost exclusively occurring below 0.04 Hz. Power in the range above 0.2 Hz was diminished, although not significantly. It is concluded that in the conscious dog, NO, as well as the baroreceptor reflex, is an effective blood pressure buffer. NO is most effective above 0.1 Hz, whereas the baroreceptors primarily buffer fluctuations slower than 0.04 Hz.

Animals↗
PubMed1993

Autoregulation and non-homeostatic behaviour of renal blood flow in conscious dogs.

1. Spontaneously occurring haemodynamic variations within 4 h affecting renal blood flow (RBF) were compared with externally induced short changes of renal artery pressure (RAP) in conscious resting dogs. 2. In all animals in which RAP was servo-controlled (n = 6), perfect autoregulation of RBF was observed. 3. In all 4 h recordings of spontaneous renal blood flow (n = 9), certain combinations of blood pressure and blood flow occurred remarkably frequently as indicated by three-dimensional frequency distributions. 4. Cluster analysis demonstrated significant differences between these areas of accumulation (P < 0.001). The average number of 'set points' per 4 h session was 3.1 +/- 0.3. 5. The shift from one set point to another is probably mediated by multiple control systems impinging on renal haemodynamics as suggested by 1/f fluctuations. 6. In seven dogs, an additional renal venous catheter allowed measurements of the arterial-venous (A-V) oxygen partial pressure (PO2) difference as an indicator of the renal metabolic demand. An inverse relationship between A-V PO2 difference and RBF (Y = X(-0.034) + 40.9, r = -0.9, P < 0.001) was found, indicating that the metabolic demands vary little (if at all) between the different set points. 7. The presented data suggest a modified view of renal homeostasis. There exist distinct combinations between RBF and RAP, which are very stable. Autoregulation merely buffers the fluctuations around these set points.

Animals↗
PubMed1993

The role of the kidney in canine blood pressure control: direct assessment of the closed-loop gain.

1. The feedback control of arterial blood pressure by the kidney in the range of hours was investigated in resting, conscious foxhounds. 2. A servo-control device (connected to an aortic occlusive cuff implanted above both renal arteries) was used to maintain a constant pressure difference of 20 mmHg between aortic pressure measured proximal (mean arterial blood pressure: MAP) and distal (renal artery pressure: RAP) to the aortic cuff. 3. Protocol 1 (n = 6) served as a 4 h time control without intervention, protocol 2 (n = 6) consisted of three periods: after a control of 20 min duration, the servo-control device was activated for 180 min; this was followed by a recovery period of 40 min. Protocol 3 (n = 6) was as protocol 2, but during converting-enzyme inhibition. 4. Servo-control increased plasma renin activity (PRA) transiently from 0.5 ng angiotensin I (AI) ml-1 h-1 to a peak value of 2.4 ng AI ml-1 h-1, subsequently both RAP and MAP rose to reach a new steady state. During this increase in RAP, PRA declined to 1.4 ng AI ml-1 h-1. 5. On average, the compensation of the pressure decrease sensed by the kidney amounted to 63% of the error signal (closed-loop gain of 0.63 +/- 0.1). 6. Converting-enzyme inhibition reduced this closed-loop gain significantly (protocol 2 vs. protocol 3, 0.63 +/- 0.1 vs. 0.15 +/- 0.1; P < 0.05). 7. It is concluded, that the kidney plays an important role in medium-term blood pressure regulation, most probably via the renin-angiotensin system.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Is arterial pressure a determinant of renal prostaglandin release?

The effect of changes in renal perfusion pressure (RPP) on renal prostaglandin (PG) release was investigated in conscious dogs (n = 10). PGE2, PGF2 alpha, and 6-keto-PGF1 alpha levels in renal venous and aortic plasma were measured in response to controlled reductions of RPP by an inflatable cuff implanted around the renal artery. PG plasma concentrations were determined by gas chromatography-negative ion chemical ionization mass spectrometry. At control RPP, PGE2 and PGF2 alpha concentrations in renal venous plasma were severalfold higher than in aortic plasma (PGE2, 54.2 +/- 13.4 vs. 9.3 +/- 2.7 pg/ml, P < 0.01; PGF2 alpha, 40.3 +/- 10.4 vs. 10.4 +/- 3.4 pg/ml, P < 0.01), whereas only a small secretion rate was found for 6-keto-PGF1 alpha (renal vein, 24.3 +/- 2.6 pg/ml; aorta, 17.4 +/- 3.4 pg/ml; P < 0.01). Concentrations of all three PGs in renal venous or aortic plasma did not change in response to reductions of RPP within the normal range of renal blood flow (RBF) autoregulation. The mean difference between PG release at a RPP of 70 mmHg and control was for PGE2 -7.9 pg/ml with a 95% confidence interval (CI) from -20.7 to + 5.0 pg/ml; for PGF2 alpha it was -13.7 pg/ml (95% CI -29.4 to +2.0 pg/ml); and for 6-keto-PGF1 alpha it was -0.9 pg/ml (95% CI -6.0 to +4.1 pg/ml). Reductions of RPP below the lower limit of RBF autoregulation (< 66 mmHg) had no effect on 6-keto-PGF1 alpha secretion rate but decreased secretion rates of PGE2 and PGF2 alpha (n = 4).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Endothelium-derived NO stimulates pressure-dependent renin release in conscious dogs.

The effect of blocking the formation of endothelium-derived relaxing factor/nitric oxide (EDNO) on pressure-dependent renin release (RR) was studied in six conscious foxhounds with chronically implanted catheters in the abdominal aorta and the renal vein. Renal blood flow (RBF) was measured with an ultrasonic transit-time flowmeter. RR was determined by multiplying the renal venous-arterial plasma renin activity difference with renal plasma flow. Renal artery pressure (RAP) was reduced in steps by a pneumatic occluder placed around the suprarenal abdominal aorta. A dose of 1,000 mg NG-nitro-L-arginine methyl ester (L-NAME) was given as a bolus to inhibit EDNO formation. In response to L-NAME, RAP increased (98 +/- 3 vs. 128 +/- 3 mmHg; P < 0.05), heart rate decreased (88 +/- 7 vs. 51 +/- 5 beats/min; P < 0.05), RBF decreased (280 +/- 19 vs. 185 +/- 24 ml/min; P < 0.05), and RR decreased (62 +/- 11 vs. 28 +/- 7 U; P < 0.05), whereas glomerular filtration rate changed little (38 +/- 3 vs. 35 +/- 4 ml/min; not significant). Below roughly 90 mmHg, RR was considerably attenuated by L-NAME as RAP was reduced in steps. At the lowest RAP (50 mmHg) RR was 1,946 +/- 406 U during control vs. 697 +/- 179 U after L-NAME (P < 0.05). Thus L-NAME inhibited pressure-dependent RR. This was especially pronounced in the low-pressure range.

Animals↗
PubMed1992

Phasic and 24-h blood pressure control by endothelium-derived relaxing factor in conscious dogs.

The effects of blocking endothelium-derived relaxing factor (EDRF) on 24-h blood pressure and heart rate (HR) were examined in six conscious freely moving foxhounds. The hypothesis tested was that shear stress-dependent EDRF release acts as a physiological blood pressure buffer. Telemetry recordings were obtained before and after the administration of the false substrate for EDRF synthesis NG-nitro-L-arginine (L-NNA, 16.5 +/- 2 mg/kg body wt iv). In response to L-NNA, mean arterial blood pressure (MAP) increased from 116 +/- 5 to 134 +/- 5 mmHg (P less than 0.01) and HR decreased from 97 +/- 6 to 68 +/- 3 beats/min over the entire 24-h period (P less than 0.01). The overall variability of MAP (as indicated by SD of frequency distribution) increased modestly from 9.5 +/- 0.4 to 11.7 +/- 1.1 mmHg (P less than 0.05). A sequential spectral analysis of blood pressure showed a 2.1-fold increase of power in the frequency range of 0.01-0.5 Hz (P less than 0.05) after L-NNA was given. In conclusion, blockade of EDRF led to a sustained hypertension throughout the whole 24-h recordings. Furthermore, EDRF acted as a physiological blood pressure buffer in the frequency range below 0.5 Hz.

Acetylcholine↗
PubMed1992

Physiological concentrations of ANP exert a dual regulatory influence on renin release in conscious dogs.

The influence of physiological increments in circulating atrial natriuretic peptide (ANP) on renin release was determined in conscious dogs. Renin stimulus-response curves (RSRCs) were obtained by controlled reductions of renal perfusion pressure (RPP) under control conditions and during intrarenal or intravenous ANP infusions. Under all experimental conditions, the RSRCs were characterized by a plateau, a threshold pressure (Pth), and a steep slope below Pth. Intrarenal ANP infusion (0.9 ng.kg-1.min-1), which induced a calculated threefold elevation of renal arterial ANP concentration (but did not change systemic arterial ANP levels), increased the slope of the RSRC by 81% (P less than 0.05) with no effect on Pth. A quantitatively similar effect on the slope of the RSRC (+90%; P less than 0.05) was observed when systemic ANP levels were raised (from 37 +/- 2 to 71 +/- 9 pg/ml; P less than 0.05) by intravenous infusions (3.6 ng.kg-1.min-1). In addition, however, intravenously infused ANP reduced Pth from 91 to 85 mmHg (P less than 0.05), which caused a complete suppression of the renin response to a reduction of RPP down to 85 mmHg. These findings indicate that ANP can inhibit renin release at physiological plasma concentrations by shifting the RSRC to a lower pressure level; this shift is mediated by a modulation of extrarenal renin control mechanisms. The direct effect of ANP on renin release is one of stimulation.

Animals↗
PubMed1992

A servo-control system for open- and closed-loop blood pressure regulation.

An electropneumatic servo-control system is described that can reduce and control arterial blood pressure in experimental animals. The device has been proved useful in the analysis of pressure-dependent physiological processes and allows the following two modes of operation: 1) a conventional open-loop setting that will reduce arterial pressure to a preselected set point and 2) a closed-loop mode that enables an adjustment to a dynamic pressure set point (i.e., the controlled pressure is reduced to a constant value below a reference pressure). A pneumatic servo-control mechanism was chosen to provide minimal control latency. The accuracy of the system under physiological conditions is well within +/- 1 mmHg. The device can be useful in a number of studies demanding a precise regulation of local arterial pressure, such as experiments on blood flow autoregulation, arterial baroreceptor reflexes, and all experiments involving the study of pressure-dependent excretory and incretory functions of the kidney. The closed-loop setting is useful for studying physiological feedback systems.

Animals↗
PubMed1992

Role of endothelium-derived relaxing factor in renal autoregulation in conscious dogs.

In six chronically instrumented, conscious dogs the hypothesis was tested that the release of endothelium-derived relaxing factor (EDRF) is important for autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). RBF was measured by a Transonic flowmeter. Renal perfusion pressure was servo-controlled by an aortic cuff. EDRF synthesis was inhibited by NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg iv). L-NAME increased mean systemic blood pressure (30 mmHg) and decreased heart rate (-40 beats/min), but it left autoregulation of RBF and GFR intact. However, basal RBF decreased markedly (2.24 +/- 0.32 ml.min-1.g-1 with L-NAME vs. 3.91 +/- 0.64 ml.min-1.g-1 for control, P less than 0.01), whereas basal GFR was not significantly influenced (0.37 +/- 0.05 ml.min-1.g-1 with L-NAME vs. 0.42 +/- 0.06 ml.min-1.g-1 for control). Hence filtration fraction increased with L-NAME [27.6 +/- 1.7% vs. 19.3 +/- 1.3% (P less than 0.01)]. The lower limit of autoregulation remained unchanged for RBF (64 +/- 5 mmHg with L-NAME vs. 63 +/- 3 mmHg for control) and increased slightly for GFR (74 +/- 2 mmHg with L-NAME vs. 67 +/- 1 mmHg for control, P less than 0.01). In conclusion, basal EDRF activity tonically influences renal resistance vessels; however, EDRF release is not primarily involved in the process of renal autoregulation. The maintenance of GFR suggests that this effect is localized in preglomerular as well as in postglomerular arterioles.

Acetylcholine↗
PubMed1991

Blood pressure control in arterial- and cardiopulmonary receptor denervated dogs.

The mechanisms influencing arterial blood pressure and heart rate were studied in conscious foxhounds after chronic sino-aortic and cardiopulmonary denervation (N = 6). In previous investigations it was shown, that this denervation produces hypertension and tachycardia, which is confirmed by the present study: Mean arterial blood pressure increased from 101 +/- 3 to 123 +/- 6 mmHg (P less than 0.05), and heart rate rose from 85 +/- 6 to 124 +/- 5 beats min-1 (P less than 0.001). The variability of mean arterial blood pressure, but not that of heart rate increased (from 6 +/- 1 to 22 +/- 2 mmHg (P less than 0.001). The administration of the alpha-adrenergic blocker prazosin reduced both mean arterial blood pressure (-33 +/- 8 mmHg, P less than 0.01) and its variability (-12 +/- 1 mmHg, P less than 0.01), thus suggesting an alpha-adrenergic mediated hypertension. beta-blockade by propranolol blunted the heart rate increase (-24 +/- 5 beats min-1, P less than 0.05). Although plasma renin activity increased in the denervated dogs, converting enzyme inhibition had little effect on mean arterial blood pressure and heart rate. In conclusion, chronic sino-aortic and cardiopulmonary denervation enhances the alpha and beta-adrenergic component of cardiovascular control in a different fashion. While the alpha-adrenergic component induces fluctuations around an elevated arterial blood pressure level, the beta-adrenergic tone to the heart increases without any significant increase in variability.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Effects of neuropeptide-Y on renal function and its interaction with sympathetic stimulation in conscious dogs.

1. The effects of neuropeptide-Y (NPY) on renal function were investigated in conscious foxhounds. 2. Dose-response curves (n = 7) were obtained for NPY by measuring renal blood flow (RBF), glomerular filtration rate (GFR), urine excretion (VU), sodium excretion (VNa), potassium excretion (VK) and plasma renin activity (PRA) at different infusion rates. All variables decreased with increasing infusion rates except for PRA, which surprisingly did not change during the different infusion rates. 3. The influence of the non-constrictor dose of NPY at control pressure, and after servo-controlling renal arterial pressure at 80 mmHg, was determined for these parameters (n = 6). 4. This was repeated during a reflex sympathetic activation via carotid sinus hypotension, in order to quantify a possible interaction between the sympathetic transmitter and co-transmitter (n = 6). 5. The subthreshold NPY dose raised plasma NPY-like immunoreactivity (NPY-LI IR) significantly (renal venous plasma: 54 +/- 13 vs. 405 +/- 117 pg ml-1; P less than 0.05) and enhanced the pressure-dependent (80 mmHg) antidiuresis (0.48 +/- 0.06 vs. 0.24 +/- 0.02 ml min-1; P less than 0.05), antinatriuresis (46 +/- 11 vs. 25 +/- 3 mumol min-1; P less than 0.05), antikaliuresis (19 +/- 4 vs. 9 +/- 0.7 mumol min-1; P less than 0.05) and pressure-dependent renin release (0.95 +/- 0.27 vs. 3.0 +/- 1.1 ng angiotensin I ml-1 h-1; P less than 0.05). These effects are consistent with a non-uniform vasoconstrictor action of NPY in the renal vascular bed (see accompanying papers). 6. The effects of NPY plus sympathetic activation were less than the sum of the two individual effects, which may rely on a presynaptic mechanism.

Animals↗
PubMed1990

Resetting of renal autoregulation in conscious dogs: angiotensin II and alpha1-adrenoceptors.

It has recently been shown, that common carotid occlusion (CCO) impairs autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). This study was designed to investigate the mechanisms by which a moderate sympathetic stimulus influences RBF and GFR autoregulation. CCO provided a moderate sympathetic stimulus, and impaired autoregulation by increasing the lower autoregulatory limit of RBF and GFR by 21-30 mmHg. Basal RBF and GFR were not affected. A low-dose intrarenal infusion of the alpha 1-adrenoceptor agonist methoxamine (which did not change total RBF or GFR) induced a similar shift as CCO (n = 5, RBF: +31 +/- 11 mmHg, P less than 0.05; GFR: +24 +/- 4 mmHg, P less than 0.01). In another group it was shown, that a combination of CCO with an intrarenal angiotensin II (A II) blockade (saralasin) did not significantly alter the response to CCO (n = 7). These data suggest an alpha 1-adrenergic pathway for the sympathetic resetting of autoregulation. An augmented A II formation does not play a major role in mediating this effect.

Adrenergic alpha-Antagonists↗
PubMed1990

Identification of major slow blood pressure oscillations in conscious dogs.

All physiological feedback systems (e.g., in arterial pressure control) tend to oscillate in a characteristic manner. Mechanoreceptors can effectively buffer resulting fluctuations in arterial blood pressure. In this study arterial and cardiopulmonary receptors were interrupted in eight conscious foxhounds by sectioning the afferent pathways to the central nervous system. In response, three major peaks were detected in the blood pressure power spectrum: in addition to the well-known rhythms reflecting heart rate and respiration, very slow oscillating waves with a cycle length of 20 +/- 4 min and a 10(5)-fold higher power than the other two waves were detected. The amplitude of these oscillations could exceed 100 mmHg. This peak was also identified under control conditions (at a cycle length of 21 +/- 4 min, n = 6); however, the relative power was greater than 10(3)-fold less with mechanoreceptors intact (P less than 0.001). Thus a major slow oscillating component of arterial pressure control has been identified. Normally, mechanoreceptors buffer the resulting waves of this oscillator. These very strong fluctuations may characterize an important feature of blood pressure regulation.

Animals↗
PubMed1990

Sympathetic modulation of renal autoregulation by carotid occlusion in conscious dogs.

The effects of a moderate reflex activation of the sympathetic nervous system on renal blood flow (RBF) and glomerular filtration rate (GFR) were studied in 29 experiments on seven conscious foxhounds. Autoregulation parameters were derived by a stepwise reduction of renal artery pressure of 10-mmHg decrements. An occlusion of both common carotid arteries (CCO) was used as a moderate sympathetic stimulus. This procedure did not influence the basal levels of RBF and GFR. However, the lower limits of autoregulation were considerably shifted (RBF, control 63 +/- 3 mmHg vs. CCO 91 +/- 8 mmHg, P less than 0.01; GFR, control 77 +/- 5 mmHg vs. CCO 102 +/- 5 mmHg, P less than 0.01). CCO also affected the rate by which RBF and GFR decreased below the autoregulatory range (subautoregulatory function: RBF, control y = 0.056x - 1.4 vs. CCO y = 0.037x - 0.9 ml.mmHg-1.g-1, P less than 0.05; GFR, control y = 0.0089x - 0.4 vs. CCO y = 0.0054x - 0.28 ml.mmHg-1.g-1, P less than 0.05). An alpha-blockade via intrarenal prazosin infusions markedly inhibited these effects of CCO. These findings demonstrate the failure of autoregulation below 102 mmHg for GFR and 91 mmHg for RBF during sympathetic activation, and they may be of clinical importance for situations that are characterized by a high sympathetic tone.

Animals↗
PubMed1990

Neurogenic control of pressure natriuresis in conscious dogs.

In this study we investigated the interaction of the sympathetic nervous system with renal perfusion pressure (RPP) in the short-term control of sodium excretion (UNa V). Pressure natriuresis curves (PNCs) were determined in 13 conscious dogs on a normal-salt diet during control conditions, bilateral common carotid occlusion (CCO), CCO combined with an intrarenal prazosin infusion, and during an intrarenal methoxamine infusion. RPP was reduced in controlled steps by inflation of a cuff placed around the renal artery. For controls, a reduction in RPP resulted in a strong decrease in urine output and UNaV. In all dogs, the PNC was closely related to individual resting blood pressure; UNaV fell to less than 50% of control (10-20 mmHg below resting blood pressure). A baroreflex activation of the sympathetic nervous system by CCO shifted PNC to the right by 10-15 mmHg (n = 8). Sensitivity of pressure natriuresis was not affected by CCO. The shift was blocked when the selective alpha 1-adrenoceptor antagonist prazosin was infused intrarenally during CCO (n = 9). Without CCO, prazosin had no effects on urine flow rate or UNaV at the control RPP. Similar to CCO, intrarenal infusion of the selective alpha 1-adrenoceptor agonist methoxamine shifted PNC to the right by 15-20 mmHg (n = 4). Neither renal blood flow nor glomerular filtration rate was significantly different between control and any experimental condition. These results indicate that the sympathetic nervous system regulates UNaV by shifting the PNC through intrarenal alpha 1-adrenoceptors without altering the sensitivity of pressure natriuresis.

Animals↗