Regional hemodynamic effects of calcitonin gene-related peptide

1989 ◽  
Vol 256 (2) ◽  
pp. R332-R338 ◽  
Author(s):  
S. M. Gardiner ◽  
A. M. Compton ◽  
T. Bennett
Keyword(s):  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Calcitonin Gene Related Peptide ◽  
Renal Vascular Resistance ◽  
High Dose ◽  
Base Line ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
The Common ◽  
Renal Vascular

Cardiovascular responses to infusions of rat alpha-calcitonin gene-related peptide (CGRP; 0.06, 0.6, 6.0 nmol/h) or rat alpha-atrial natriuretic peptide (ANP; 3.7 nmol/h) were measured in conscious rats. During infusion of the low dose of CGRP, when mean arterial pressure (MAP) was little affected, there were reductions in common carotid, renal, mesenteric, and hindquarter vascular resistances (the magnitude of the responses in the same descending order). However, only flow in the common carotid vessels was increased above base line. After infusion, there was a hindquarter vasoconstriction. During infusion of the higher doses of CGRP, there were dose-related decreases in MAP and increases in heart rate associated with (hyperemic) hindquarter vasodilatations and mesenteric vasoconstrictions. The common carotid vasodilatation peaked with the intermediate dose of CGRP; the changes in renal vascular resistance were not dose related. After infusion of the high dose of CGRP there were persistent (at least 60 min) common carotid and hindquarter vasodilatations and mesenteric vasoconstriction, with a transient overshoot in renal vascular resistance. Infusions of CGRP and ANP matched for their effects on MAP had similar influences on mesenteric hemodynamics, but all other variables were affected differently.

scholarly journals High‐dose phenylephrine increases meningeal blood flow through TRPV1 receptor activation and release of calcitonin gene‐related peptide

2019 ◽  
Vol 24 (2) ◽  
pp. 383-397 ◽  
Author(s):  
Mária Dux ◽  
Alexandru Babes ◽  
Jessica Manchen ◽  
Julika Sertel‐Nakajima ◽  
Birgit Vogler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Receptor Activation ◽  
Calcitonin Gene Related Peptide ◽  
High Dose ◽  
Trpv1 Receptor ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Meningeal Blood Flow ◽  
Flow Through

Effects of renal perfusion pressure on the natriuresis induced by atrial natriuretic factor

1987 ◽  
Vol 253 (2) ◽  
pp. F234-F238
Author(s):  
A. A. Seymour ◽  
S. G. Smith ◽  
E. K. Mazack
Keyword(s):  
Vascular Resistance ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Base Line ◽  
Renal Perfusion Pressure ◽  
Natriuretic Factor ◽  
Renal Vascular ◽  
Atrial Natriuretic

Synthetic atrial natriuretic factor (ANF 101-126) was infused at 1, 5, 25, and 125 pmol X kg-1 X min-1 into the renal artery of anesthetized, one-kidney dogs. During administration of 25 and 125 pmol X kg-1 X min-1 of ANF 101-126, fractional sodium excretion (FENa) rose from 1.4 +/- 0.3 to 6.6 +/- 1.1 and 5.6 +/- 1.3% when renal perfusion pressure (RPP) was at its basal level (112 +/- 5 mmHg). When base-line RPP was lowered to 101 +/- 5 mmHg by tightening a suprarenal aortic constriction, the same doses raised FENa to only 5.6 +/- 1.6 and 5.1 +/- 1.6%. A larger reduction of beginning RPP to 82 +/- 4 mmHg suppressed the natriuretic responses to 25 and 125 pmol X kg-1 X min-1 of ANF 101-126 to only 1.4 +/- 0.8 and 0.8 +/- 0.3%, respectively.During the peak natriuretic dose of 25 pmol X kg-1 X min-1, renal vascular resistance (RVR) fell from 0.88 +/- 0.10 to 0.68 +/- 0.07, from 0.78 +/- 0.10 to 0.68 +/- 0.12, and from 0.60 +/- 0.06 to 0.61 +/- 0.06 mmHg X ml-1 X min-1 at RPP = RPP = 112, 101, and 82 mmHg, respectively. ANF 101-126 did not affect glomerular filtration rate (GFR) at any level of RPP tested. In conclusion, the natriuretic responses to ANF 101-126 occurred without changes in GFR and were modulated by the prevailing levels of renal perfusion pressure and renal vascular resistance.

Increased Calcitonin Gene-Related Peptide and Macrophages Are Involved in Astragalus membranaceus-Mediated Peripheral Nerve Regeneration in Rats

2018 ◽  
Vol 46 (01) ◽  
pp. 69-86 ◽  
Author(s):  
Chung-Chia Chen ◽  
Ling-Chuan Chang ◽  
Chun-Hsu Yao ◽  
Yuan-Man Hsu ◽  
Jia-Horng Lin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Calcitonin Gene Related Peptide ◽  
Astragalus Membranaceus ◽  
High Dose ◽  
Nerve Growth ◽  
Expression Levels ◽  
Related Peptide ◽  
Calcitonin Gene

Astragalus membranaceus (AM) is one of 50 fundamental herbs in traditional Chinese medicine. Previous studies have shown that AM extract can be a potential nerve growth-promoting factor, being beneficial for the growth of peripheral nerve axons. We further investigated the effects of AM extract on regeneration in a rat sciatic nerve transection model. Rats were divided into three groups ([Formula: see text]): normal saline (intraperitoneal) as the control, and 1.5[Formula: see text]g/kg or 3.0[Formula: see text]g/kg of AM extract (every other day for four weeks), respectively. We evaluated neuronal electrophysiology, neuronal connectivity, macrophage infiltration, expression levels and location of calcitonin gene-related peptide (CGRP), and expression levels of both nerve growth factors (NGFs) and immunoregulatory factors. In the high-dose AM group, neuronal electrophysiological function (measured by nerve conductive velocity and its latency) was significantly improved ([Formula: see text]). Expression levels of CGRP and macrophage density were also drastically enhanced ([Formula: see text]). Expression levels of fibroblast growth factor (FGF), NGF, platelet-derived growth factor (PDGF), transforming growth factor-[Formula: see text], interleukin-1 (IL-1), and interferon (IFN)-[Formula: see text] were reduced in the high-dose AM group ([Formula: see text]), while FGF, NGF, PDGF, IL-1, and IFN-[Formula: see text] were increased in the low-dose AM group ([Formula: see text]). These results suggest that AM can modulate local inflammatory conditions, enhance nerve regeneration, and potentially increase recovery of a severe peripheral nerve injury.

Renal protection by a dual ETA/ETB endothelin antagonist, L-754,142, after aortic cross-clamping in the dog.

1997 ◽  
Vol 8 (7) ◽  
pp. 1061-1071 ◽  
Author(s):  
S M Krause ◽  
T F Walsh ◽  
W J Greenlee ◽  
R Ranaei ◽  
D L Williams ◽  
...  
Keyword(s):  
Renal Insufficiency ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Sodium Reabsorption ◽  
High Dose ◽  
Renal Protection ◽  
Suprarenal Aorta ◽  
Renal Vascular ◽  
Endothelin Antagonist

Renal insufficiency is a significant complication that occurs after surgical procedures, requiring cross-clamping of the aorta. The mechanism for this renal dysfunction is currently not known, but studies suggest a potential role of endothelin in mediating the insufficiency. Accordingly, the role of endothelin was assessed using the nonpeptidyl, dual ETA/ETB endothelin antagonist L-754,142 in a model of renal insufficiency in the anesthetized dog induced by cross-clamping the suprarenal aorta for 60 min, followed by 2 h of reperfusion. In vehicle-treated animals (saline, n = 8) after 2 h of reperfusion, plasma [ET-1] increased 66% and renal blood flow (RBF) was reduced by 38% compared with baseline. This decline was associated with an 84% increase in renal vascular resistance and a 54% reduction in GFR (baseline, 46 +/- 5 ml/min; 21 +/- 3 ml/min at 2 h; P < 0.01) and sodium reabsorption (baseline, 6.7 +/- 0.7 microEq/min; 3.0 +/- 0.5 microEq/min at 2 h, P < 0.01). After baseline measurements, pretreatment with L-754,142 at 0.3 mg/kg bolus + 0.1 mg/kg per h continuous infusion (low dose; n = 8) or 3.0 mg/kg bolus + 1 mg/kg per h infusion (high dose; n = 8) initiated 45 min before aortic cross-clamp led to a dose-dependent normalization of RBF and renal vascular resistance within 2 h of cross-clamp removal. GFR was also improved and returned to within 75% of baseline (P < 0.01 versus vehicle) by 2 h of reperfusion with L-754,142 (baseline, 55 +/- 5 ml/min; 42 +/- 5 ml/min at 2 h with the high dose). The improvement of GFR with L-754,142 treatment was associated with a preservation of sodium reabsorption compared with vehicle-treated animals. This study supports a role of endothelin in the pathogenesis of renal insufficiency after aortic cross-clamping and demonstrates that pretreatment with the dual ETA/ETB endothelin antagonist L-754,142 preserves RBF and sodium reabsorption, leading to a significant improvement in GFR.

Cardiovascular effects of calcitonin gene-related peptide in conscious dogs

1989 ◽  
Vol 257 (4) ◽  
pp. R726-R731 ◽  
Author(s):  
B. C. Wang ◽  
P. Bie ◽  
R. J. Leadley ◽  
K. L. Goetz
Keyword(s):  
Infusion Rate ◽  
Beta Blockers ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Calcitonin Gene Related Peptide ◽  
Right Atrial ◽  
Separate Experiment ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Dose Dependent

To elucidate the cardiovascular effects of alpha-human calcitonin gene-related peptide (CGRP), we infused CGRP intravenously at increasing rates of 3, 10, and 30 pmol.kg-1.min-1 during successive 15-min intervals into intact dogs, cardiac-denervated (CD) dogs, and cardiac-denervated dogs pretreated with beta-blockers. In intact dogs, the initial infusion rate of CGRP at 3 pmol.kg-1.min-1 did not produce significant hemodynamic changes, but the two higher infusion rates produced dose-dependent decreases in total peripheral resistance, mean arterial pressure, and left and right atrial pressures and produced dose-dependent increases in heart rate (HR) and cardiac output (CO). In addition, stroke volume decreased and pulmonary vascular resistance increased at the highest infusion rate. In CD dogs, CGRP produced qualitatively similar responses, although the increase in HR was markedly attenuated. The increase in CO was also attenuated, but the difference did not reach statistical significance. In CD dogs pretreated with beta-blockers, CGRP did not increase HR and the increase in CO was further attenuated. In a separate experiment, the lowest dose of CGRP (3 pmol.kg-1.min-1) was infused intravenously for 60 min in intact dogs; significant cardiovascular responses, qualitatively similar to those produced by higher rates of infusion, occurred. We conclude that CGRP is an extremely potent vasodilator and that the increase in HR is mediated primarily by autonomic reflexes.

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