AN EXTRA-ADRENAL EFFECT OF CORTICOTROPHIN

1967 ◽  
Vol 37 (3) ◽  
pp. 245-252 ◽  
Author(s):  
E. STARK ◽  
B. VARGA ◽  
ZS. ÁCS
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Commercial Preparation ◽  
Naturally Occurring ◽  
Dose Dependent

SUMMARY Administered intravenously, a commercial preparation of naturally occurring corticotrophin as well as synthetic corticotrophin were found to raise ovarian blood flow both in the normal and in the adrenalectomized dog and cat, without affecting systemic blood pressure. Peaks and periods of time for which flow remained increased were dose-dependent.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

Excessive Zinc Intake Increases Systemic Blood Pressure and Reduces Renal Blood Flow via Kidney Angiotensin II in Rats

2012 ◽  
Vol 150 (1-3) ◽  
pp. 285-290 ◽  
Author(s):  
Miyoko Kasai ◽  
Takashi Miyazaki ◽  
Tsuneo Takenaka ◽  
Hiroyuki Yanagisawa ◽  
Hiromichi Suzuki
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Zinc Intake

scholarly journals Characterization and cardiovascular actions of endothelin-1 and endothelin-3 from the American alligator

2002 ◽  
Vol 282 (2) ◽  
pp. R594-R602 ◽  
Author(s):  
Björn Platzack ◽  
Yuqi Wang ◽  
Dane Crossley ◽  
Valentine Lance ◽  
James W. Hicks ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Biological Activities ◽  
Systemic Blood Pressure ◽  
Second Phase ◽  
Systemic Blood ◽  
Cardiovascular Actions ◽  
Dose Dependent Decrease ◽  
Alligator Mississipiensis ◽  
Dose Dependent

The structures and biological activities of the isoforms of endothelin (ET) in a reptile are unknown. ET-3, whose primary structure is identical to human ET-3 except for the substitution Phe4 → Tyr, and a peptide identical to human ET-1 were isolated from an extract of the lung of the alligator, Alligator mississipiensis. Bolus intravenous injections of alligator ET-3 (10, 30, and 100 pmol/kg) into anesthetized alligators produced dose-dependent decreases in systemic blood pressure (Psys) and systemic vascular resistance (Rsys) without change in heart rate (HR), systemic blood flow (Qsys), pulmonary pressure (Ppul), pulmonary vascular resistance (Rpul), or pulmonary blood flow (Qpul). At a dose of 300 pmol/kg, the initial vasodilatation was followed by an increase in Rsys and decreases in Qsys and Ppul. The response to intravenous human/alligator ET-1 (10, 30, 100, and 300 pmol/kg) was biphasic at all doses with initial decreases in Psys and Rsys being followed by sustained increases in these parameters. In the pulmonary circulation, ET-1 produced a dose-dependent decrease in Qpul and an increase in Rpul during the first phase of the response but no significant change during the second phase. There was no change in HR in response to ET-1. The vasodilatator action of arginine, but not ET-1, was attenuated by N ω-nitro-l-arginine methyl ester, indicating that the effect of the peptide is probably not mediated through increased synthesis of nitric oxide. The data demonstrate that the structure of the ET isoforms has been strongly conserved during the evolution of vertebrates but that cardiovascular actions differ significantly between the alligator and mammals, especially in the magnitude and duration of the hypotensive response.

Skeletal muscle vasodilation at the onset of exercise

1998 ◽  
Vol 85 (5) ◽  
pp. 1649-1654 ◽  
Author(s):  
John B. Buckwalter ◽  
Stephen B. Ruble ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscarinic Receptors ◽  
Treadmill Exercise ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Iliac Arteries ◽  
Blood Flows ◽  
Peak Blood

The purpose of this study was to determine whether β-adrenergic or muscarinic receptors are involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs ( n = 7) were instrumented with flow probes on both external iliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 μg), both drugs, or saline was infused intra-arterially immediately before treadmill exercise at 3 miles/h, 0% grade. Immediate and rapid increases in iliac blood flow occurred with initiation of exercise under all conditions. Peak blood flows were not significantly different among conditions (682 ± 35, 646 ± 49, 637 ± 68, and 705 ± 50 ml/min, respectively). Although the doses of antagonists employed had no effect on heart rate or systemic blood pressure, they were adequate to abolish agonist-induced increases in iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of β-adrenergic and muscarinic receptors is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs.

Baroreceptor influence on postural changes in blood pressure and carotid blood flow

1963 ◽  
Vol 205 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Francis L. Abel ◽  
John H. Pierce ◽  
Warren G. Guntheroth
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Sinus ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Carotid Blood Flow ◽  
Postural Changes ◽  
Nembutal Anesthesia

The effects of 30° head-down and head-up tilting on mean systemic blood pressure, carotid blood flow, and heart rate were studied in 16 dogs under morphine and Nembutal anesthesia. The tilting procedure was further repeated after denervation of the carotid sinus and aortic arch baroreceptors and after administration of a dihydrogenated ergot alkaloid mixture (Hydergine). The results indicate that the drop in pressure in the head-down position is primarily due to baroreceptor activity and that the baroreceptors are necessary for compensatory vasoconstriction on head-up tilting. Carotid blood flow decreased in both tilted positions in the control animals; the possible relationship to cerebral blood flow is discussed.

scholarly journals Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice

2018 ◽  
Vol 19 (4) ◽  
pp. 967 ◽  
Author(s):  
Evanthia Mergia ◽  
Manuel Thieme ◽  
Henning Hoch ◽  
Georgios Daniil ◽  
Lydia Hering ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Guanylyl Cyclase ◽  
Systemic Blood Pressure ◽  
Systemic Blood
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