Role of secretin and CCK in the stimulation of pancreatic secretion in conscious dogs. Effects of atropine and somatostatin

1987 ◽  
Vol 2 (4) ◽  
pp. 223-235
Author(s):  
Stanislaw J. Konturek ◽  
JanW Konturek ◽  
Cornelis B. Lamers ◽  
Janine Tasler ◽  
Jan Bilski
Keyword(s):  
Pancreatic Secretion ◽  
Conscious Dogs ◽  
Stimulation Of

Role of EDRF/NO in parasympathetic coronary vasodilation following carotid chemoreflex activation in conscious dogs

1994 ◽  
Vol 267 (2) ◽  
pp. H605-H613 ◽  
Author(s):  
W. Shen ◽  
M. Ochoa ◽  
X. Xu ◽  
J. Wang ◽  
T. H. Hintze
Keyword(s):  
Vagus Nerve ◽  
Conscious Dogs ◽  
Coronary Resistance ◽  
Vascular Response ◽  
Coronary Vasodilation ◽  
Relaxing Factor ◽  
Anesthetized Dogs ◽  
Endothelium Derived Relaxing Factor ◽  
Stimulation Of

The role of endothelium-derived relaxing factor (EDRF) in parasympathetic coronary vasodilation following carotid chemoreflex activation induced by nicotine in conscious dogs and stimulation of the vagus nerve in anesthetized dogs was studied. Injection of nicotine (11 +/- 4 micrograms) into the carotid artery increased coronary blood flow (CBF) by 126 +/- 16% from 28 +/- 3 ml/min and reduced late diastolic coronary resistance (LDCR) by 43 +/- 4% from 3.58 +/- 0.52 mmHg.ml-1.min, accompanied by a significant increase in mean arterial pressure and a decrease in heart rate (all P < 0.01). Pacing and propranolol did not change the coronary vascular response to chemoreflex activation. There were still increases in CBF by 113 +/- 17% from 29 +/- 3 ml/min and decreases in LDCR by 41 +/- 5% from 3.13 +/- 0.52 mmHg.ml-1.min (all P < 0.01). After infusion of N omega-nitro-L-arginine (L-NNA) (30 mg/kg), the increase in CBF following chemoreflex activation was only 23 +/- 3% from 37 +/- 3 ml/min, and the fall in LDCR was 19 +/- 3% from 3.09 +/- 0.51 mmHg.ml-1.min. Stimulation of the vagus nerve showed a relationship between stimulation frequency and coronary vasodilation that was significantly inhibited by L-NNA. Thus EDRF plays an important role in mediating parasympathetic coronary vasodilation during chemoreflex activation and perhaps during many reflexes that cause vagal cholinergic vasodilation in the heart.

Assessing baroreflex gain from spontaneous variability in conscious dogs: role of causality and respiration

2000 ◽  
Vol 279 (5) ◽  
pp. H2558-H2567 ◽  
Author(s):  
A. Porta ◽  
G. Baselli ◽  
O. Rimoldi ◽  
A. Malliani ◽  
M. Pagani
Keyword(s):  
High Frequency ◽  
Low Frequency ◽  
Systolic Arterial Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Parametric Models ◽  
Conscious Dogs ◽  
Regulatory Mechanisms ◽  
Stimulation Of

A double exogenous autoregressive (XXAR) causal parametric model was used to estimate the baroreflex gain (αXXAR) from spontaneous R-R interval and systolic arterial pressure (SAP) variabilities in conscious dogs. This model takes into account 1) effects of current and past SAP variations on the R-R interval (i.e., baroreflex-mediated influences), 2) specific perturbations affecting R-R interval independently of baroreflex circuit (e.g., rhythmic neural inputs modulating R-R interval independently of SAP at frequencies slower than respiration), and 3) influences of respiration-related sources acting independently of baroreflex pathway (e.g., rhythmic neural inputs modulating R-R interval independently of SAP at respiratory rate, including the effect of stimulation of low-pressure receptors). Under control conditions, αXXAR = 14.7 ± 7.2 ms/mmHg. It decreases after nitroglycerine infusion and coronary artery occlusion, even though the decrease is significant only after nitroglycerine, and it is completely abolished by total arterial baroreceptor denervation. Moreover, αXXAR is comparable to or significantly smaller than (depending on the experimental condition) the baroreflex gains derived from sequence, power spectrum [at low frequency (LF) and high frequency (HF)], and cross-spectrum (at LF and HF) analyses and from less complex causal parametric models, thus demonstrating that simpler estimates may be biased by the contemporaneous presence of regulatory mechanisms other than baroreflex mechanisms.

Role of vasopressin in stimulation of ACTH secretion by angiotensin II in conscious dogs

1986 ◽  
Vol 251 (1) ◽  
pp. E52-E57
Author(s):  
C. K. Klingbeil ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Conscious Dogs ◽  
Ang Ii ◽  
Acth Secretion ◽  
Series Of Experiments ◽  
Stimulation Of ◽  
Acth Release

Three series of experiments were performed in conscious dogs to test the possibility that the stimulation of adrenocorticotropin (ACTH) release by angiotensin II (ANG II) is mediated by arginine vasopressin (AVP). In the first protocol, the effect of ANG II on ACTH release was studied in dogs in which endogenous AVP levels had been increased by water deprivation. Water deprivation for 24 h increased plasma AVP concentration from 3.0 +/- 0.5 to 7.7 +/- 0.5 pg/ml (P less than 0.01) and increased the AVP response to the highest dose of ANG II (20 ng X kg-1 X min-1). Despite these changes, water deprivation failed to increase the ACTH response to ANG II. Next, the contribution of endogenous AVP to the stimulation of ACTH release by ANG II was examined using the V1-receptor antagonist, d(CH2)5Tyr[Met]-AVP (10 micrograms/kg iv). The ACTH response to ANG II in the presence of the AVP antagonist (66.4 +/- 3.1 to 100.1 +/- 15.9 pg/ml) was not significantly less than that in its absence (53.0 +/- 4.8 to 72.2 +/- 11.1 pg/ml). Finally, ANG II and AVP were infused in combination to determine whether there is a synergism between these two peptides in the release of ACTH. In one protocol, AVP and ANG II were infused separately and in combination. The ACTH response to ANG II and AVP in combination (48.7 +/- 6.5 to 61.5 +/- 8.5 pg/ml) was not enhanced compared with the responses to ANG II (59.8 +/- 7.3 to 71.0 +/- 10.1 pg/ml) or AVP (48.8 +/- 5.7 to 55.6 +/- 6.5 pg/ml) alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Biphasic secretory response of exocrine pancreas to feeding

1980 ◽  
Vol 238 (4) ◽  
pp. G332-G337 ◽  
Author(s):  
Z. Itoh ◽  
R. Honda ◽  
K. Hiwatashi
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Pancreas ◽  
Physiological Role ◽  
Secretory Response ◽  
Conscious Dogs ◽  
Bicarbonate Secretion ◽  
Secretory Pattern ◽  
Second Peak

By means of a newly developed device, secretory response of the exocrine pancreas to feeding was continuously recorded for 24 h in conscious dogs. It was then found that the postprandial secretory pattern of the pancreas was biphasic. The first peak of secretion, rich in enzymes, occurred 2.3 +/- 0.11 h after feeding and its secretory volume was 25.3 +/- 3.10 ml/h. After the first peak, pancreatic secretion decreased slightly, but started to increase again. At 10.8 +/- 0.31 h after feeding, the second peak of secretion occurred and this was 40.5 +/- 2.93 ml/h, significantly higher than the first peak secretion and the greatest in 1 day. The second peak secretion did not contain a higher concentration of enzymes, but was rich in bicarbonate. Approximately 16 h after feeding, pancreatic secretion returned to the basal level, which continued until the next meal. That water and bicarbonate secretion of the pancreas is the greatest at about the 11th postprandial h had never been reported before. The physiological role of the pancreatic secretion at that time is more likely to be related to the neutralization of acid entering from the stomach than to the digestion of food.

Vasoactive intestinal polypeptide in vagally mediated pancreatic secretion of fluid and HCO3.

1979 ◽  
Vol 237 (6) ◽  
pp. E535 ◽  
Author(s):  
J Fahrenkrug ◽  
O B Schaffalitzky de Muckadell ◽  
J J Holst ◽  
S L Jensen
Keyword(s):  
Electrical Stimulation ◽  
Vasoactive Intestinal Polypeptide ◽  
Pancreatic Secretion ◽  
Vagal Stimulation ◽  
Porcine Pancreas ◽  
Pancreatic Fluid ◽  
Stimulation Of ◽  
Intestinal Polypeptide

The role of nerves that liberate vasoactive intestinal polypeptide (VIP) in the porcine pancrease as mediators of the atropine-resistant action of the vagus on flow and bicarbonate (HCO3) secretion was examined. Efferent electrical stimulation of the vagus in atropinized pigs produced a profuse flow of pancreatic juice with high HCO3 content concomitantly with a significant increase in pancreatic VIP output from 13 to 113 fmol/min. Intravenous administration of somatostatin (SRIF) during continuous electrical vagal stimulation caused a parallel suppression of the VIP release and the pancreatic fluid and HCO3 secretion to prestimulatory values. The SRIF-induced reduction in fluid and HCO3 secretion seemed to be mediated via an inhibition of the VIP release rather than through a direct effect on the exocrine cells, inasmuch as SRIF did not influence the VIP-provoked exocrine response from the in vitro isolated perfused porcine pancreas. The results support the view that VIP is transmitter in the vagally induced atropine-resistant water and HCO3 secretion from the porcine pancreas.

Effects of CRF and ANG II on ACTH and vasopressin release in conscious dogs

1988 ◽  
Vol 255 (1) ◽  
pp. E46-E53 ◽  
Author(s):  
C. K. Klingbeil ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Conscious Dogs ◽  
Ang Ii ◽  
Plasma Acth ◽  
Vasopressin Release ◽  
Intravenous Saline ◽  
Acth Concentration ◽  
Dose Dependent ◽  
Stimulation Of ◽  
Acth Release

The aim of the present study was to examine the effects of corticotropin-releasing factor (CRF) in conscious dogs and to determine whether the stimulation of adrenocorticotropic hormone (ACTH) release by angiotensin II (ANG II) results from potentiation of the action of CRF. In addition, the possible role of CRF in the stimulation of vasopressin released by ANG II was investigated. The following experiments were performed: 1) intravenous saline infusion; 2) ANG II (10 ng.kg-1.min-1) alone; 3) vasopressin (1 ng.kg-1.min-1) alone; 4) CRF (0.001, 0.01, or 0.1 microgram/kg iv) bolus; 5) vasopressin (1 ng.kg-1.min-1) and CRF (0.1 microgram/kg) together; 6) CRF (0.001, 0.01, or 0.1 microgram/kg) and ANG II (10 ng.kg-1.min-1) together; 7) ANG II (10 ng.kg-1.min-1) followed 15 min later with CRF (0.001, 0.01, or 0.1 microgram/kg). Each dose of CRF was tested on a different day. Infusion of ANG II alone stimulated the release of ACTH, cortisol, and vasopressin. Administration of CRF produced dose-dependent increases in plasma ACTH and cortisol concentrations, and the highest dose of CRF increased plasma vasopressin concentration. CRF given together with ANG II did not potentiate the stimulation of ACTH release by CRF. Vasopressin at the dose tested did not stimulate ACTH release but potentiated the ACTH response to CRF. ANG II stimulated vasopressin release but did not potentiate the AVP response to CRF. These results show that, in conscious dogs, ANG II and CRF each increase plasma ACTH concentration and that the ACTH response to CRF is potentiated by vasopressin but not by ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

Role of gluconeogenesis in sustaining glucose production during hypoglycemia caused by continuous insulin infusion in conscious dogs

Diabetes ◽  
1988 ◽  
Vol 37 (6) ◽  
pp. 749-759 ◽  
Author(s):  
R. T. Frizzell ◽  
G. K. Hendrick ◽  
D. W. Biggers ◽  
D. B. Lacy ◽  
D. P. Donahue ◽  
...  
Keyword(s):  
Insulin Infusion ◽  
Glucose Production ◽  
Conscious Dogs ◽  
Continuous Insulin Infusion
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