REDUCTION OF CIRCULATING INSULIN LEVELS DURING THE INFUSION OF DIFFERENT PROSTAGLANDINS IN THE RAT

1975 ◽  
Vol 79 (1) ◽  
pp. 266-274 ◽  
Author(s):  
L. Saccà ◽  
G. Perez ◽  
F. Rengo ◽  
I. Pascucci ◽  
M. Condorelli
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Insulin Response ◽  
Inhibitory Effect ◽  
Receptor System ◽  
Insulin Levels ◽  
Arterial Blood ◽  
Post Infusion ◽  
Plasma Insulin Levels ◽  
Pre Treatment

ABSTRACT The intravenous infusion of prostaglandin (PG) E1, E2, and A1 into normal rats at a dose of 2 μg/min significantly lowered plasma insulin levels with a tendency to recovery in the post-infusion period. Whereas PGA1 infusion resulted in a moderate but significant hypoglycaemia, the administration of E-series PGs always produced a hyperglycaemic effect. The interference of PGE1 on insulin response to classical insulinogogues (glucagon, aminophylline, and tolbutamide) was also investigated. The results of these experiments demonstrate that PGE1 exerts an inhibitory action on insulin response to all insulin releasing agents investigated. As regards the haemodynamic effects of PGs, PGE1 and PGE2 lowered the arterial blood pressure by about 20%, while PGA1 was almost completely ineffective. On the other hand, the lowering effect of PGE1 on circulating insulin levels remained unchanged in rats treated with reserpine. These findings thus rule out a sympathetic over-activity secondary to the lowered arterial blood pressure as the mechanism of action of PGE1. A possible direct interference with the adrenergic receptor system of the pancreatic islets was also ruled out since the inhibitory effect of PGE1 was not overcome by phentolamine pre-treatment.

scholarly journals Rostral ventral medulla 5-HT1A receptors selectively inhibit the somatosympathetic reflex

2001 ◽  
Vol 280 (5) ◽  
pp. R1261-R1268 ◽  
Author(s):  
Takashi Miyawaki ◽  
Ann K. Goodchild ◽  
Paul M. Pilowsky
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Potent Inhibition ◽  
Somatosympathetic Reflex

The role of the 5-hydroxytryptamine (5-HT1A) receptors in the rostral ventrolateral medulla (RVLM) on somatosympathetic, baroreceptor, and chemoreceptor reflexes was examined in anesthetized rats. Microinjection of the selective 5-HT1A agonist 8-hydroxy-di- n-propylamino tetralin (8-OH-DPAT) decreased arterial blood pressure and splanchnic sympathetic nerve activity (SNA). Electrical stimulation of the hindlimb evoked early and late excitatory sympathetic responses. Bilateral microinjection in the RVLM of 8-OH-DPAT markedly attenuated both the early and late responses. This potent inhibition of the somatosympathetic reflex persisted even after SNA and arterial blood pressure returned to preinjection levels. Preinjection of the selective 5-HT1A antagonist NAN-190 in the RVLM blocked the sympathoinhibitory effect of 8-OH-DPAT and attenuated the inhibitory effect on the somatosympathetic reflex. 8-OH-DPAT injected in the RVLM did not affect baroreceptor or chemoreceptor reflexes. Our findings suggest that activation of 5-HT1A receptors in the RVLM exerts a potent, selective inhibition on the somatosympathetic reflex.

scholarly journals Influence of endurance training on central sympathetic outflow to skeletal muscle in response to a mixed meal

2010 ◽  
Vol 108 (4) ◽  
pp. 882-890 ◽  
Author(s):  
Colin N. Young ◽  
Shekhar H. Deo ◽  
Areum Kim ◽  
Masahiro Horiuchi ◽  
Catherine R. Mikus ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endurance Training ◽  
Arterial Blood Pressure ◽  
Plasma Insulin ◽  
Muscle Sympathetic Nerve Activity ◽  
Insulin Response ◽  
Sympathetic Outflow ◽  
Mixed Meal ◽  
Arterial Blood ◽  
Central Sympathetic Outflow

Nutrient intake is accompanied by increases in central sympathetic outflow, a response that has been mainly attributed to insulin. Insulin-mediated sympathoexcitation appears to be blunted in insulin-resistant conditions, suggesting that aside from peripheral insulin insensitivity, such conditions may also impair the central action of insulin in mediating sympathetic activation. What remains unclear is whether an insulin-sensitive state, such as that induced by chronic endurance training, alters the central sympathetic effects of insulin during postprandial conditions. To examine this question plasma insulin and glucose, muscle sympathetic nerve activity (MSNA), heart rate, and arterial blood pressure were measured in 11 high-fit [HF; peak oxygen uptake (V̇o2peak) 65.9 ± 1.4 ml·kg−1·min−1] and 9 average-fit (AF; V̇o2peak 43.6 ± 1.3 ml·kg−1·min−1) male subjects before and for 120 min after ingestion of a mixed meal drink. As expected, the insulin response to meal ingestion was lower in HF than AF participants (insulin area under the curve0–120: 2,314 ± 171 vs. 4,028 ± 460 μIU·ml−1·120−1, HF vs. AF, P < 0.05), with similar plasma glucose responses between groups. Importantly, following consumption of the meal, the HF subjects demonstrated a greater rise in MSNA compared with the AF subjects (e.g., 120 min: Δ21 ± 1 vs. 8 ± 3 bursts/100 heart beats, HF vs. AF, P < 0.05). Furthermore, when expressed relative to plasma insulin, HF subjects exhibited a greater change in MSNA for any given change in insulin. Arterial blood pressure responses following meal intake were similar between groups. Collectively, these data suggest that, in addition to improved peripheral insulin sensitivity, endurance training may enhance the central sympathetic effect of insulin to increase MSNA following consumption of a mixed meal.

Arterial baroreceptors mediate the inhibitory effect of acute increases in arterial blood pressure on thirst

2002 ◽  
Vol 282 (6) ◽  
pp. R1718-R1729 ◽  
Author(s):  
Sean D. Stocker ◽  
Edward M. Stricker ◽  
Alan F. Sved
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Drinking Behavior ◽  
Plasma Osmolality ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Arterial Blood ◽  
Acute Increase ◽  
Behavior Of Rats ◽  
Arterial Baroreceptor

The present study sought to determine whether arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in arterial blood pressure (AP) on thirst stimulated by systemically administered ANG II or by hyperosmolality. Approximately 2 wk after sinoaortic denervation, one of four doses of ANG II (10, 40, 100, or 250 ng · kg−1 · min−1) was infused intravenously in control and complete sinoaortic-denervated (SAD) rats. Complete SAD rats ingested more water than control rats when infused with 40, 100, or 250 ng · kg−1 · min−1 ANG II. Furthermore, complete SAD rats displayed significantly shorter latencies to drink compared with control rats. In a separate group of rats, drinking behavior was stimulated by increases in plasma osmolality, and mean AP was raised by an infusion of phenylephrine (PE). The infusion of PE significantly reduced water intake and lengthened the latencies to drink in control rats but not in complete SAD rats. In all experiments, drinking behavior of rats that were subjected to sinoaortic denervation surgery but had residual baroreceptor reflex function (partial SAD rats) was similar to that of control rats. Thus it appears that arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in AP on thirst stimulated by ANG II or hyperosmolality.

Naloxone enhances the increase in plasma growth hormone induced by α2-adrenergic stimulation in healthy males

1987 ◽  
Vol 114 (2) ◽  
pp. 308-313 ◽  
Author(s):  
Margareta Bramnert ◽  
Bernt Hökfelt
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Adrenergic Stimulation ◽  
Arterial Blood ◽  
Normotensive Subjects ◽  
Pre Treatment ◽  
Plasma Gh ◽  
Single Blind ◽  
Healthy Males

Abstract. There is evidence that the α2-adrenergic agonist clonidine interacts with the opioid system. In the present investigations, the effect of naloxone on the increase in plasma GH induced by clonidine and the more specific α2-agonist guanfacine was studied in man. In a single-blind study, five healthy males received in randomized order either the preservatives in the naloxone preparation (control) or naloxone at two different doses (10 or 100 μg/kg) followed by an infusion of either diluted preservatives or naloxone (5 or 50 μg · kg−1 · h−1, respectively). Fifteen min after the bolus dose, clonidine (3 μg/kg) or guanfacine (15 μg/kg) was infused over 10 min in a single-blind order. Both clonidine and guanfacine induced an increase in plasma GH (P < 0.05), Pre-treatment with naloxone at the higher dosage resulted in an enhanced (P < 0.05) GH response to clonidine and guanfacine, respectively, whereas the lower dosage of naloxone was without effect. The increase in plasma GH did not correlate with basal mean arterial blood pressure, nor with the changes in mean arterial blood pressure induced by clonidine or guanfacine. These results indicate that the increase in plasma GH induced by α2-adrenergic stimulation in normotensive subjects involves opioid receptors with moderate sensitivity to naloxone.

Acute Haemodynamic and Hormonal Effects of Captopril are Diminished by Indomethacin

1982 ◽  
Vol 62 (6) ◽  
pp. 611-615 ◽  
Author(s):  
H. Witzgall ◽  
F. Hirsch ◽  
B. Scherer ◽  
P. C. Weber
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Plasma Renin ◽  
Hormonal Effects ◽  
Arterial Blood ◽  
Before And After ◽  
Pre Treatment ◽  
Excretion Rates

1. The acute haemodynamic and hormonal effects of 100 mg of captopril (SQ 14.225) orally were tested in twelve healthy men in the sodium replete state before and after indomethacin pre-treatment. 2. Without indomethacin, mean arterial blood pressure was reduced at 30 and 60 min after captopril (P < 0.02). Heart rate did not change during the whole experiment. Although plasma renin activity (PRA) increased (P < 0.002), plasma and urinary aldosterone and plasma 18-hydroxycorticosterone (18-OH-B) decreased after captopril (P < 0.02). Prostaglandin (PG) E2, sodium and potassium excretion rates remained constant after captopril. 3. Under indomethacin pretreatment, the fall in mean arterial blood pressure was less than without indomethacin at 30 and 60 min after captopril (P < 0.05). Heart rate was constantly lower than without indomethacin during the whole experiment (P < 0.05). Indomethacin pretreatment decreased basal PGE2 excretion (P < 0.02) and baseline PRA as well as the increase in PRA after captopril (P < 0.05). Control mineralocorticoid levels were significantly lower than without indomethacin. In indomethacin-pretreated subjects, aldosterone did not further decrease after captopril, and 18-OH-B fell only slightly. 4. Without indomethacin pretreatment a significant, positive correlation was found between PRA values before captopril and the maximum decrease of mean arterial blood pressure after captopril. Under indomethacin pretreatment this correlation was no longer demonstrable. The results suggest that prostaglandins may contribute to the haemodynamic and hormonal actions of captopril.

Cardiovascular Effects of Micromeria graeca (L.) Benth. ex Rchb in Normotensive and Hypertensive Rats

2020 ◽  
Vol 20 (8) ◽  
pp. 1253-1261
Author(s):  
Mourad Akdad ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Cardiovascular System ◽  
Arterial Blood Pressure ◽  
Antihypertensive Activity ◽  
Computer Assisted ◽  
Hypertensive Rats ◽  
Vasorelaxant Effect ◽  
Arterial Blood

Aims: The present study was performed in order to analyze the antihypertensive activity of Micromeria graeca (L.) Benth. ex Rchb. Background: Micromeria graeca (L.) Benth. ex Rchb is an aromatic and medicinal plant belonging to the Lamiaceae family. This herb is used to treat various pathologies such as cardiovascular disorders. Meanwhile, its pharmacological effects on the cardiovascular system have not been studied. Objective: The present study aimed to evaluate the effect of aqueous extract of aerial parts of Micromeria graeca (AEMG) on the cardiovascular system in normotensive and hypertensive rats. Methods: In this study, the cardiovascular effect of AEMG was evaluated using in vivo and in vitro investigations. In order to assess the acute effect of AEMG on the cardiovascular system, anesthetized L-NAME-hypertensive and normotensive rats received AEMG (100 mg/kg) orally and arterial blood pressure parameters were monitored during six hours. In the sub-chronic study, rats were orally treated for one week, followed by blood pressure assessment during one week of treatment. Blood pressure was measured using a tail-cuff and a computer-assisted monitoring device. In the second experiment, isolated rat aortic ring pre-contracted with Epinephrine (EP) or KCl was used to assess the vasorelaxant effect of AEMG. Results: Oral administration of AEMG (100 mg/kg) provoked a decrease of arterial blood pressure parameters in hypertensive rats. In addition, AEMG induced a vasorelaxant effect in thoracic aortic rings pre-contracted with EP (10 μM) or KCl (80 mM). This effect was attenuated in the presence of propranolol and methylene blue. While in the presence of glibenclamide, L-NAME, nifedipine or Indomethacin, the vasorelaxant effect was not affected. Conclusion: This study showed that Micromeria graeca possesses a potent antihypertensive effect and relaxes the vascular smooth muscle through β-adrenergic and cGMP pathways.

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