Increased alpha 1-adrenergic vascular sensitivity during development of hypertension in conscious dogs

1993 ◽  
Vol 264 (4) ◽  
pp. H1259-H1268 ◽  
Author(s):  
N. Uemura ◽  
D. E. Vatner ◽  
Y. T. Shen ◽  
J. Wang ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Conscious Dogs ◽  
Aortic Tissue ◽  
Ang Ii ◽  
Receptor Density ◽  
Adrenergic Stimulation ◽  
Before And After ◽  
Vascular Responsiveness

The goal of this study was to determine whether enhanced vascular responsiveness during the development of perinephritic hypertension is selective or nonspecific. The effects of graded infusions of norepinephrine (NE), phenylephrine (PE), angiotensin II (ANG II), and vasopressin (VP) were examined on mean arterial pressure, total peripheral resistance (TPR), and aortic pressure-diameter relationships in conscious dogs. NE increased TPR significantly greater (P < 0.01) in hypertension than normotension, as did PE infusion, whereas ANG II and VP increased TPR similarly before and after hypertension. Analysis of aortic pressure-diameter relationships also demonstrated significant (P < 0.05) shifts in response to NE and PE, but not ANG II and VP, during the development of hypertension. In normotensive dogs, low doses of ANG II infusion also enhanced the vasoconstrictor response not only to NE and PE but also to VP. In contrast to what was observed in hypertension, in the presence of ANG II infusion after ganglionic blockade, enhanced responses to PE and NE were no longer observed. The alpha 1-adrenergic receptor density in membrane preparations from aortic tissue, as determined by [3H]prazosin binding, was higher (P < 0.05) in hypertensive dogs than control dogs. Thus the vascular responsiveness in the aorta and resistance vessels is enhanced to alpha 1-adrenergic stimulation, but not to all vasoconstrictors, during developing perinephritic hypertension. The mechanism appears to involve increased alpha 1-adrenergic receptor density.

Changes in vascular responsiveness following chronic exposure to cold in the rat

1983 ◽  
Vol 55 (3) ◽  
pp. 823-829 ◽  
Author(s):  
B. A. Bryar ◽  
M. J. Fregly ◽  
F. P. Field
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscles ◽  
Aortic Tissue ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Aortic Smooth Muscle ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Vascular Responsiveness ◽  
High Concentrations

The responsiveness of smooth muscle from rings of aortic tissue of cold-acclimated (CA, 6 degrees C, 5-15 wk) rats to both alpha- and beta-adrenergic agonists and KCl was tested and compared with that of warm-adapted (25 degrees C) controls. alpha-Adrenergic stimulation, induced by low doses (10(-8)-10(-7) M) of phenylephrine and norepinephrine in the presence and absence of the beta-adrenergic antagonist, propranolol, resulted in the development of less active tension by aortic smooth muscle from CA rats than from controls. Similar results were observed with the weakly alpha 1-adrenergic agonistic activities of tyramine, clonidine, and high concentrations of isoproterenol (10(-6)-10(-4) M). There was also a significant reduction in the tension developed by smooth muscles of the aortas from CA rats when depolarized with KCl in concentrations ranging from 8 to 20 mM. In contrast, aortic smooth muscle, contracted to 75% of maximum with KCl, showed an enhanced relaxation to the beta-adrenergic agonist, isoproterenol, in CA rats. These studies suggest that acclimation of rats to cold results in both a decrease in alpha-adrenergic responsiveness and an increase in beta-adrenergic responsiveness in vascular smooth muscle as well as a change in the biochemical events that couple activation of adrenergic receptors to changes in vasomotor tone.

Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension

2001 ◽  
Vol 281 (6) ◽  
pp. H2511-H2517 ◽  
Author(s):  
Ming Yu ◽  
Venkat Gopalakrishnan ◽  
Thomas W. Wilson ◽  
J. Robert McNeill
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hemodynamic Responses ◽  
Hypertensive Group ◽  
Time Flow ◽  
Before And After ◽  
Vascular Responsiveness

The contribution of endothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension.

Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs

1984 ◽  
Vol 247 (6) ◽  
pp. F881-F887 ◽  
Author(s):  
L. C. Gregory ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Reflex Response ◽  
Renal Nerves ◽  
Ang Ii ◽  
Before And After

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

In vivo aortic wall characteristics at the early stage of atherosclerosis in rabbits

1997 ◽  
Vol 273 (3) ◽  
pp. H1142-H1147 ◽  
Author(s):  
K. Hironaka ◽  
M. Yano ◽  
M. Kohno ◽  
T. Tanigawa ◽  
M. Obayashi ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Aortic Wall ◽  
Early Stage ◽  
Aortic Pressure ◽  
Normal Diet ◽  
Acute Administration ◽  
Wide Range ◽  
Before And After ◽  
Vascular Responsiveness

To assess whether vascular responsiveness to alpha-receptor agonist is altered at the early stage of atherosclerosis, in vivo aortic pressure-diameter relationship of the aorta over a wide range of pressures was analyzed before and after the acute administration of alpha-receptor agonist (phenylephrine) in nine hypercholesterolemic fat-fed (7-wk-old) rabbits and eight normal diet-fed (7-wk-old) rabbits. In hypercholesterolemic fat-fed rabbits, there was no major structural change in the aortic wall except fatty streak, despite a marked increase in the level of plasma cholesterol, indicating the early stage of atherosclerosis of the aorta. By using a modified three-element Maxwell model, diastolic stress-strain relationship was computed after applying several assumptions to the actual aortic pressure-diameter relationship. After the intravenous administration of phenylephrine at a rate of 5 micrograms.kg-1.min-1, the stress (ordinate)-strain (abscissa) relationship curves were shifted to the left, indicating the activation of aortic smooth muscle by phenylephrine. The difference between the stress before and after phenylephrine showed a single peak at a certain strain. The peak difference in the stress was smaller in hypercholesterolemic fat-fed rabbits than in normal diet-fed rabbits, indicating the reduction of vascular responsiveness at the early stage of atherosclerosis of the aorta.

Skeletal muscle beta-adrenoceptor distribution and responses to isoproterenol in hyperthyroidism

1992 ◽  
Vol 262 (4) ◽  
pp. E504-E510 ◽  
Author(s):  
W. H. Martin ◽  
E. Korte ◽  
T. K. Tolley ◽  
J. E. Saffitz
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptor ◽  
Human Skeletal Muscle ◽  
Muscle Fibers ◽  
Type I ◽  
Receptor Density ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Isoproterenol Infusion

To determine whether hyperthyroidism selectively increases beta-adrenergic receptor density in vessels or fibers of human skeletal muscle, we characterized beta-receptor distribution autoradiographically in muscle biopsies of 18 subjects aged 26 +/- 1 yr before and after daily administration of 100 micrograms 3,5,3'-triiodothyronine (T3) for 2 wk. To establish whether vascular and metabolic responses to beta-adrenergic stimulation are concomitantly altered, we quantified calf blood flow and plasma concentrations of glucose, lactate, glycerol, free fatty acids (FFA), insulin, and C-peptide during graded-dose isoproterenol infusion in eight of these individuals. Differences in beta-adrenergic receptor density among muscle fiber types and vascular components were highly significant (type I greater than type IIa greater than type IIb muscle fibers, P less than 0.001; and type I muscle fibers greater than resistance arterioles, P less than 0.05). Hyperthyroidism increased beta-adrenergic receptor density in all types of muscle fibers (+31-50%; P less than 0.01) but not in resistance arterioles. There was no change in calf blood flow or plasma glucose, glycerol, FFA, insulin, or C-peptide responses to isoproterenol. A rise in lactate during stages 3 and 4 of isoproterenol infusion (P less than 0.01) was observed before but not after T3 administration. Thus hyperthyroidism increases beta-adrenergic receptor density in fibers but not vessels of human skeletal muscle without increasing either metabolic or vascular responses to selective beta-adrenergic stimulation.

Enhanced left ventricular shortening during chronic volume overload in conscious dogs

1980 ◽  
Vol 238 (2) ◽  
pp. H126-H133 ◽  
Author(s):  
M. M. LeWinter ◽  
R. L. Engler ◽  
J. S. Karliner
Keyword(s):  
Volume Overload ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Stimulation ◽  
Ventricular Performance ◽  
Blood Pressure Elevation ◽  
Chronic Volume Overload ◽  
Before And After ◽  
Ejection Phase

Prior work with the arteriovenous fistula model indicates that left ventricular performance is at least normal and may be enhanced during chronic volume overload. The present study was undertaken in conscious dogs to determine whether ejection-phase indices of ventricular function are enhanced after 1 mo of volume overload, using an experimental design in which loading conditions could be accounted for and animals were used as their own controls before and after volume overload. We also examined the response of the volume-overloaded left ventricle to an afterload stress and the role of adrenergic stimulation in maintenance of function. Both at rest and during hemodynamically matched conditions, percent shortening (ultrasonic dimension gauges) and mean shortening rates were increased during volume overload. This difference was maintained during phenylephrine-induced blood pressure elevation, although diastolic dimensions increased more in control studies during phenylephrine. Propranolol produced significantly larger reductions in these indices during volume overload than in the control state. Thus, ejection-phase function is enhanced during volume overload, at least in part due to increased adrenergic stimulation.

Splenic contraction-induced increases in arterial O2 reduce requirement for CBF in conscious dogs

1995 ◽  
Vol 269 (2) ◽  
pp. H491-H503 ◽  
Author(s):  
N. Sato ◽  
Y. T. Shen ◽  
K. Kiuchi ◽  
R. P. Shannon ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Conscious State ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Sympathomimetic Amines ◽  
Blood Flows ◽  
Before And After ◽  
Myocardial O2 Consumption ◽  
Consequent Increase ◽  
Adrenergic Receptor Blockade

We investigated the extent to which sympathomimetic amines induced splenic contraction and associated increases in arterial O2 content (CaO2) and how these mechanisms affected control of the coronary circulation by sympathomimetic amines in conscious dogs. Blood hemoglobin (Hb) and CaO2 increased by 16 +/- 2 and 18 +/- 2%, respectively, during norepinephrine (NE, 0.8 micrograms.kg-1.min-1 iv) in the intact, conscious state after splenic contraction. Phenylephrine (PE) induced similar effects. After either alpha 1-adrenergic-receptor blockade or splenectomy, these effects were abolished. Isoproterenol (Iso) also decreased splenic thickness, which was abolished after ganglionic, alpha-, or beta 1/beta 2-adrenergic-receptor blockade. Direct infusions of NE and PE into the splenic artery decreased splenic thickness and increased Hb and CaO2, whereas Iso had no effect. After splenectomy, NE did not increase CaO2, but coronary blood flow (CBF) increased more (73 +/- 6%) vs. before splenectomy (49 +/- 7%) without any differences before and after splenectomy in the responses of pressures, contractility, and myocardial O2 consumption (MVO2). In contrast, renal, mesenteric, and iliac artery blood flows were not significantly different in response to sympathomimetic amines before and after splenectomy. These data indicate that sympathomimetic amines induced splenic contraction either directly or reflexly via alpha-adrenergic-receptor stimulation. The consequent increase in Hb and CaO2 allows for equivalent increases in MVO2, but at a smaller increase in CBF.

Effects of α- and β-adrenergic receptor stimulation and oxytocin receptor blockade on milking characteristics in dairy cows before and after removal of the teat sphincter

2003 ◽  
Vol 70 (3) ◽  
pp. 289-292 ◽  
Author(s):  
Tyra Inderwies ◽  
Johannes Riedl ◽  
Evangelos Kiossis ◽  
Rupert M. Bruckmaier
Keyword(s):  
Milk Yield ◽  
Adrenergic Receptor ◽  
Peak Flow ◽  
Muscle Tone ◽  
Blocking Agent ◽  
Receptor Blockade ◽  
Adrenergic Stimulation ◽  
Receptor Stimulation ◽  
Milk Flow ◽  
Before And After

Alpha (α)- and beta (β)-adrenergic receptors in the bovine mammary gland are mainly present in the teat muscles and in the region where large milk ducts reach the cisternal cavities. The aim of the study was to test the hypothesis that the region of the large mammary ducts is the most important location of α- and β-adrenergic receptor stimulation affecting milk ejection and milk removal. Effects of α- and β-adrenergic receptor stimulation and of oxytocin (OT) receptor blockade on milking characteristics were tested in six cows. Milk flow was measured before and after the distal part of one teat, including the teat canal and teat sphincter, had been partly amputated. Before the operation, milk yield and peak flow rate decreased during α-adrenergic receptor stimulation and during the OT receptor blockade, and increased during β-adrenergic stimulation. After removal of the teat tip, relations of milk yield and peak flow rates after administration of α- and β-agonists and after application of an OT receptor blocking agent were similar to those before operation. Only total milk yield had decreased in the teat-amputated quarter owing to unhindered flow of cisternal milk before cluster attachment. Since responses to α- and β-adrenergic receptor stimulation as well as to OT receptor blockade do not differ with or without the teat sphincter, it is concluded that milk flow is mainly influenced by the muscle tone of the large mammary ducts.

Regulation of drinking and vasopressin secretion: role of organum vasculosum laminae terminalis

1987 ◽  
Vol 253 (1) ◽  
pp. R108-R120 ◽  
Author(s):  
T. N. Thrasher ◽  
L. C. Keil
Keyword(s):  
Conscious Dogs ◽  
Ang Ii ◽  
Cellular Dehydration ◽  
Organum Vasculosum Laminae Terminalis ◽  
Before And After ◽  
Electrolytic Ablation ◽  
Vasopressin Secretion ◽  
Osmotic Stimulus ◽  
Organum Vasculosum

We have proposed that the organum vasculosum laminae terminalis (OVLT) contains osmoreceptors involved in the regulation of drinking and secretion of arginine vasopressin (AVP) in the dog. By use of the technique of electrolytic ablation, conscious dogs were evaluated for their responses to acute peripheral challenges of hypertonic NaCl and angiotensin II (ANG II) and hemorrhage (20 ml/kg) before and after destruction of the OVLT (n = 7) or adjacent tissue (n = 9) as a control. Lesions confined to the tip of the optic recess and destroying greater than 90% of the OVLT caused a dramatic increase in the threshold to drink and increase plasma AVP levels and a significant (P less than 0.01) reduction in the magnitude of these responses to an osmotic stimulus. Drinking and secretion of AVP in response to ANG II, but not the rise in peripheral corticosteroids, were also blocked (P less than 0.01) by ablation of the OVLT. In contrast responses to hemorrhage were not affected by the lesion. These results support the hypothesis that the OVLT contains osmoreceptors involved in physiological responses to cellular dehydration and suggest involvement in drinking and secretion of AVP in response to ANG II. The results also indicate that forebrain mechanisms which depend on the OVLT are independent of mechanisms responding to hemorrhage in conscious dogs.

Endurance training in dogs increases vascular responsiveness to an alpha 1-agonist

1988 ◽  
Vol 65 (2) ◽  
pp. 625-632 ◽  
Author(s):  
Y. M. Evans ◽  
J. N. Funk ◽  
J. B. Charles ◽  
D. C. Randall ◽  
C. F. Knapp
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Central Venous Pressure ◽  
Endurance Training ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Central Venous ◽  
Vascular Responsiveness

The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. Aortic pressure, cardiac output, central venous pressure, peripheral resistance, and heart rate were each averaged over 30 s before injection and 90 s after injection. The slope of the peripheral resistance-dose relationship was significantly increased in trained compared with untrained dogs in both the unblocked and blocked cases [unblocked: trained 0.89, untrained 0.47; blocked: trained 4.30, untrained 2.05 (mmHg.l-1.min)/(microgram.kg-1)]. The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.

Sign in / Sign up

Export Citation Format

Share Document