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P Persson

Publications and source records attributed to P Persson.

68 records · Page 4Linked to original sources
PubMed1988

Cholecystokinins but not gastrin-17 release calcitonin from thyroid C-cells in the rat.

Subcutaneous injections of gastrin-17, cholecystokinin-39, cholecystokinin-8 (sulfated and non-sulfated forms), cholecystokinin-4 or pentagastrin induced hypocalcemia in rats. The hypocalcemia was associated with calcitonin release for pentagastrin and the cholecystokinins but not for gastrin-17, even at very high doses. Permanent hypergastrinemia, induced by surgical removal of the acid-producing part of the stomach (fundectomy) or by treatment with high doses of omeprazole, a blocker of acid secretion, was not accompanied by elevated plasma calcitonin. Long-lasting hypergastrinemia is known to cause hyperplasia of gastrin-sensitive endocrine cells in the rat stomach while hypogastrinemia does the reverse. In antrectomized rats, having low serum gastrin, and in fundectomized rats, having high serum gastrin, the serum calcitonin concentration, the thyroid calcitonin content and the number of C-cells remained as in sham-operated controls two months after the operations. We conclude that neither exogenous nor endogenous gastrin stimulates calcitonin secretion in the rat and that long-standing hypo- or hypergastrinemia is without effect on the number of thyroid C-cells. Our results, however, do not exclude the possibility that the cholecystokinins might act as calcitonin secretagogues in the rat although such a role remains to be established.

Animals↗
PubMed1988

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↗
PubMed1988

Cardiopulmonary receptors and "neurogenic hypertension".

The intention of the present studies was to analyze the effects of arterial baroreceptors and cardiopulmonary receptors on cardiovascular control (I,IV,VI) and renin release (I,II,IV,V). The investigations of the role of the renin-angiotensin system on arterial pressure (III,VII) were applied to interpret a possible contribution to "neurogenic hypertension". Following conclusions are made by our findings: The partial or complete denervation of one receptor area leads to no changes in long-term arterial pressure, heart rate, plasma volume, or plasma renin activity. After sino-aortic denervation only a higher blood pressure variability is observed. Total denervation of both receptor sites increases blood pressure and its lability as well as the heart rate, although the heart rate variability remains the same. The information from arterial baroreceptors and cardiopulmonary receptors is redundant: both have an attenuating effect on the cardiovascular system but the input is not additive. "Neurogenic hypertension" is due to the denervation of both arterial baroreceptors and cardiopulmonary receptors. Arterial baroreceptor denervation alone will only increase blood pressure fluctuations. The pathway of this form of hypertension is alpha-adrenergic, the tachycardia is mediated via beta-receptors. A major role of the renin-angiotensin system or plasma volume regulation is not evident. Plasma renin activity is significantly increased, but converting-enzyme inhibition shows no obvious effect on "neurogenic hypertension". A tissue angiotensin II facilitation of the beta-adrenergic elevation of heart rate seen after total denervation is not apparent. No changes of heart rate were observed after converting-enzyme inhibition.

Animals↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1987

Pharmacokinetics of midazolam in total i.v. anaesthesia.

The pharmacokinetics of midazolam during total i.v. anaesthesia were determined in 15 female patients undergoing major surgery. Midazolam was administered together with an analgesic drug and a neuromuscular blocking drug. The dose regimen of midazolam, based on simulations, included two consecutive infusions following a bolus injection at the induction of anaesthesia. Multiple blood samples were drawn and a two-compartment open model was fitted to the measured plasma concentrations. Plasma clearance (483 ml min-1), apparent volume of distribution (1.94 litre kg-1) and terminal half-life (3.1 h) were in agreement with other reports. Thus, there was no obvious evidence that the surgical procedure or the concomitant use of other drugs, or both, influenced the pharmacokinetics of midazolam. The relatively rapid elimination makes midazolam suitable for use by infusion in a total i.v. technique.

Adult↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1986

Midazolam-fentanyl anesthesia for major surgery. Plasma levels of midazolam during prolonged total intravenous anesthesia.

The water-soluble benzodiazepine midazolam was used along with fentanyl and pancuronium in a totally intravenous anesthetic technique for hysterectomies. Midazolam was given as a 0.3 mg X kg-1 bolus dose followed by constant rate infusion of 0.25 mg X kg-1 X h-1. Plasma midazolam concentrations were measured during the anesthesia. The technique provided excellent conditions for surgery, with pulse rate and blood pressure under good control and without any recall of the peri-operative period. A disadvantage was early respiratory depression, which necessitated administration of naloxone to make extubation possible. This was attributed to the proportionally large amount of fentanyl used. Drowsiness during the first postoperative hours was also pronounced.

Adult↗
PubMed1985

Baroreflex sympathetic activation increases threshold pressure for the pressure-dependent renin release in conscious dogs.

Stimulus-response curves relating renal-venous-arterial plasma renin activity difference (P.R.A.-difference) to mean renal artery pressure (R.A.P.) were studied in seven chronically instrumented conscious foxhounds with a daily sodium intake of 6.1 mmol/kg. R.A.P. was reduced in steps and maintained constant for 5 min using an inflatable renal artery cuff and a pressure control system. The stimulus-response curve obtained during control conditions (C) or during common carotid artery occlusion (C.C.O.) could be approximated by two linear sections: a rather flat section or plateau-level of P.R.A.-difference at normal blood pressure or above, and a very steep section between a distinct threshold pressure and 65-70 mm Hg. While the parameters of the curves varied from dog to dog, the curves kept their unique shape in the individual dog for at least 1 week. C.C.O. had no effect on the plateau-level of the P.R.A.-difference (C:0.98 +/- 0.14, C.C.O:0.99 +/- 0.14 ng AI . ml-1 . h-1) and on the slope of the curve below threshold pressure (C:-0.379 +/- 0.041, C.C.O:-0.416 +/- 0.082 ng AI . ml-1 . h-1 . mm Hg-1) but shifted the stimulus-response curve to the right and increased threshold pressure (C:92.7 +/- 2.8, C.C.O:109.7 +/- 4.1 mm Hg; P less than 0.05). Renal blood flow, which was measured simultaneously in three of the dogs, showed good autoregulation down to 70 mm Hg under resting conditions and was not affected by C.C.O. except for a 30% reduction of renal blood flow at the lowest pressure step (70 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Studies on the retina and the pigment epithelium in hereditary canine ceroid lipofuscinosis. IV. Changes in the electroretinogram and the standing potential of the eye.

The present study correlates ultrastructural abnormalities in the retinal pigment epithelium (RPE) with electrophysiologic changes demonstrated in examinations of dogs with canine ceroid-lipofuscinosis (CCL) at various stages of clinical involvement using dc electroretinograms (ERG), including the c-wave, as well as recordings of the variations of the standing potential (SP) of the eye, both of which reflect the activity of the pigment epithelium. Normal c-waves and SP variations were seen at early stages of disease. At later stages, specific signs of pigment epithelial impairment were found in the form of (1) markedly reduced SP variations, (2) an increase in amplitude of the trough after the b-wave, and (3) a disappearance of the c-wave, which was replaced by a negative potential. These ERG changes correlate very well with a damaged pigment epithelium that generates the positive potential of the c-wave, as well as with normal Müller cells that generates the negative potential coinciding in time with the c-wave, and contributing to the trough after the b-wave. In the end-stage of the disease all potentials of the ERG were reduced drastically, evidently as a sign of cessation of neuroretinal function. Similarities between English setters with CCL and human Batten disease are discussed.

Animals↗