scholarly journals Monoaminergic Receptors as Modulators of the Perivascular Sympathetic and Sensory CGRPergic Outflows

2020 ◽  
Vol 18 (9) ◽  
pp. 790-808
Author(s):  
Bruno A. Marichal-Cancino ◽  
Abimael González-Hernández ◽  
Enriqueta Muñoz-Islas ◽  
Carlos M. Villalón
Keyword(s):  
Blood Pressure ◽  
Blood Vessels ◽  
Peripheral Vascular ◽  
Cardiovascular Parameter ◽  
Body Tissues ◽  
Pithed Rats ◽  
Calcitonin Gene ◽  
Adequate Blood Supply ◽  
Sensory Fibers ◽  
Monoaminergic Mechanisms

Blood pressure is a highly controlled cardiovascular parameter that normally guarantees an adequate blood supply to all body tissues. This parameter is mainly regulated by peripheral vascular resistance and is maintained by local mediators (i.e., autacoids), and by the nervous and endocrine systems. Regarding the nervous system, blood pressure can be modulated at the central level by regulating the autonomic output. However, at peripheral level, there exists a modulation by activation of prejunctional monoaminergic receptors in autonomic- or sensory-perivascular fibers. These modulatory mechanisms on resistance blood vessels exert an effect on the release of neuroactive substances from the autonomic or sensory fibers that modify blood pressure. Certainly, resistance blood vessels are innervated by perivascular: (i) autonomic sympathetic fibers (producing vasoconstriction mainly by noradrenaline release); and (ii) peptidergic sensory fibers [producing vasodilatation mainly by calcitonin gene-related peptide (CGRP) release]. In the last years, by using pithed rats, several monoaminergic mechanisms for controlling both the sympathetic and sensory perivascular outflows have been elucidated. Additionally, several studies have shown the functions of many monoaminergic auto-receptors and hetero-receptors expressed on perivascular fibers that modulate neurotransmitter release. On this basis, the present review: (i) summarizes the modulation of the peripheral vascular tone by adrenergic, serotoninergic, dopaminergic, and histaminergic receptors on perivascular autonomic (sympathetic) and sensory fibers, and (ii) highlights that these monoaminergic receptors are potential therapeutic targets for the development of novel medications to treat cardiovascular diseases (with some of them explored in clinical trials or already in clinical use).

Peripheral vascular responses during carotid baroreceptor stimulation in normotensive and hypertensive subjects

1987 ◽  
Vol 73 (6) ◽  
pp. 635-640 ◽  
Author(s):  
D. Duprez ◽  
N. De Pue ◽  
D. L. Clement
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Essential Hypertension ◽  
Blood Vessels ◽  
Venous Occlusion ◽  
Peripheral Vascular ◽  
Carotid Baroreceptors ◽  
Arterial Blood ◽  
Carotid Baroreceptor ◽  
Normotensive Subjects

1. The carotid baroreceptors were stimulated for 2 min by neck suction at −30 and −60 mmHg in 19 normotensive subjects and 12 patients with moderate essential hypertension. 2. Blood pressure was measured with a mercury sphygmomanometer and heart rate was derived from beat-to-beat analysis of the electrocardiogram. Blood flow was measured simultaneously at calf and finger with venous occlusion plethysmography and the vascular resistance was calculated. 3. During neck suction at − 30 and − 60 mmHg there was a significant decrease in arterial blood pressure and heart rate. There was a transient vasodilatation of the calf blood vessels, while there was a sustained vasoconstriction of the finger blood vessels. These results were qualitatively similar in both groups; however, there were quantitative differences. 4. These experiments show that there is a selective autonomic control of the different peripheral vascular beds by the carotid baroreceptors in both normotension and mild essential hypertension.

Living Well to Keep Your Pressure Down

EDIS ◽  
2017 ◽  
Vol 2017 (6) ◽  
Author(s):  
Linda B. Bobroff
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Blood Vessels ◽  
High Blood Pressure ◽  
Health Problems ◽  
Fact Sheet ◽  
Living Well ◽  
Heart Work ◽  
Major Revision ◽  
Reduce Risk

High blood pressure, or hypertension, can cause serious health problems. It makes your heart work harder and can damage your blood vessels even if you feel okay. Everyone should have their blood pressure checked regularly. If you have certain risk factors, you are more likely to have high blood pressure. This 6-page fact sheet is a major revision that discusses risk factors and ways to reduce risk.

COMPARISON OF ANTIHYPERTENSIVE EFFECT OF MOXONIDINE VERSUS CLONIDINE IN RENAL FAILURE PATIENTS.

2018 ◽  
Vol 6 (9) ◽  
Author(s):  
DR.MATHEW GEORGE ◽  
DR.LINCY JOSEPH ◽  
MRS.DEEPTHI MATHEW ◽  
ALISHA MARIA SHAJI ◽  
BIJI JOSEPH ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Blood Flow ◽  
Blood Vessel ◽  
Blood Vessels ◽  
High Blood Pressure ◽  
Antihypertensive Effect ◽  
The Body ◽  
Ability To Work ◽  
Blood Flows

Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. Factors that can increase this force include higher blood volume due to extra fluid in the blood and blood vessels that are narrow, stiff, or clogged(1). High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.

scholarly journals Vascular-ventricular coupling during exercise is not affected by exaggerated blood pressures in endurance-trained athletes

2019 ◽  
Vol 127 (3) ◽  
pp. 753-759 ◽  
Author(s):  
Katharine D. Currie ◽  
Zion Sasson ◽  
Jack M. Goodman
Keyword(s):  
Blood Pressure ◽  
Vascular Function ◽  
Arterial Compliance ◽  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Peripheral Vascular ◽  
Arterial Elastance ◽  
Coupling Index ◽  
Cardiovascular Performance ◽  
Stage 1

This study sought to examine whether cardiovascular performance during exercise, assessed using the vascular-ventricular coupling index (VVC), was affected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. Subjects were middle-aged endurance-trained men and women. Blood pressure measurements and left ventricular echocardiography were performed in a semiupright position at rest and during steady-state cycling at workloads that elicited 100–110 beats/min ( stage 1) and 130–140 beats/min ( stage 2). These data were used to calculate effective arterial elastance index ( EaI), left ventricular end-systolic elastance index ( ELVI), and their ratio (VVC). Additional measurements of left ventricular volumes and function (i.e., stroke volume, cardiac output, and longitudinal strain) and indirect assessments of peripheral vascular function (i.e., total arterial compliance and peripheral vascular resistance) were examined. Fourteen subjects with EBP (EBP+, 50% men) and 14 sex-matched subjects without EBP (EBP−) participated, with results presented as EBP+ versus EBP−. EaI and ELVI increased from rest to exercise while VVC decreased, but only ELVI was different between groups at stage 1 [7.6 (1.8) vs. 6.4 (1.0) mmHg·ml−1·m−2, P = 0.045] and stage 2 [10.3 (1.6) vs. 8.0 (1.7) mmHg·ml−1·m−2, P < 0.001]. Additional comparisons revealed no group difference in the contribution of the Frank-Starling mechanism or left ventricular and peripheral vascular function during exercise. The cardiovascular adjustment to exercise in athletes with EBP is achieved through a matched increase in both EaI and ELVI, and the absence of between-group differences in left ventricular or peripheral vascular function suggests that other factors may contribute to the EBP response. NEW & NOTEWORTHY Cardiovascular performance during submaximal exercise, assessed using vascular-ventricular coupling, is unaffected by exaggerated blood pressure (EBP) responses in endurance-trained athletes. The underlying mechanisms of EBP in athletes remain unknown as changes in left ventricular and peripheral vascular function during exercise were similar in athletes with and without EBP.

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

A New Calcitonin-Receptor-like Sequence in Rat Pulmonary Blood Vessels

1993 ◽  
Vol 85 (4) ◽  
pp. 385-388 ◽  
Author(s):  
F. Njuki ◽  
C. G. Nicholl ◽  
A. Howard ◽  
J. C. W. Mak ◽  
P. J. Barnes ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Vascular Tone ◽  
Islet Amyloid Polypeptide ◽  
Calcitonin Gene Related Peptide ◽  
Binding Activity ◽  
Calcitonin Receptor ◽  
Islet Amyloid ◽  
Related Peptide ◽  
Calcitonin Gene

1. Two rat clones have been isolated which are similar to known calcitonin-receptor sequences. One of these does not have the distribution expected of a calcitonin receptor. It is widely distributed, with extremely high levels of expression in the lung, where it is associated with the blood vessels. 2. This rat sequence may represent the receptor for calcitonin-gene-related peptide or islet amyloid polypeptide. Both have binding activity in the lung and are potent vasodilators. The gene represented by this sequence may therefore play an important role in the maintenance of vascular tone.

Duvadilan

1964 ◽  
Vol 2 (9) ◽  
pp. 33-34
Keyword(s):  
Vascular Disease ◽  
Blood Vessels ◽  
Peripheral Vascular Disease ◽  
Premature Labour ◽  
Peripheral Vascular ◽  
Recent Issue ◽  
Sympathomimetic Amine

Isoxsuprine, a sympathomimetic amine marketed by Crookes (Duvadilan) and Qrganon (Dilavase), inhibits contractions of the uterus and dilates blood vessels. Crookes recommend its use to arrest premature labour, and paradoxically also to accelerate labour at term and to overcome cervical rigidity. Both firms promote isoxsuprine as a vasodilator for use in peripheral vascular disease; we discussed this aspect of the drug in a recent issue.1

Abstract 17638: Systemic Cardiovascular Effects of Intravenous Urocortin 2 and Urocortin 3 in Patients with Heart Failure and Healthy Volunteers

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Colin G Stirrat ◽  
Sowmya Venkatasubramanian ◽  
Tania Pawade ◽  
Andrew Mitchell ◽  
Anoop Shah ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Cardiac Index ◽  
Healthy Volunteers ◽  
Diastolic Blood Pressure ◽  
Cardiovascular Effects ◽  
Peripheral Vascular ◽  
Patients With Heart Failure ◽  
Group A ◽  
Urocortin 3

Introduction: Urocortin 2 (UCN 2) and urocortin 3 (UCN 3) are endogenous peptide hormones with an emerging role in the pathophysiology and treatment of heart failure. For the first time, we examined the systemic cardiovascular effects of both UCN 2 and UCN 3 in healthy volunteers and patients with heart failure. Methods: Seven healthy volunteers (Group A) and nine patients with stable chronic heart failure (Group B, New York Heart Association class II and III, left ventricular ejection fraction <35%) on optimal medical therapy underwent non-invasive oscillometric sphygmomanometry and impedance cardiography during incremental intravenous infusions of sodium nitroprusside (0.15/0.5/1.5 μg/kg/min), UCN 2 (0.16/0.48/1.6 μg/min), UCN 3 (5/15/50 μg/min) and saline placebo in a randomised double blind two-way cross over study. Results: Other than diastolic blood pressure (78 vs 72 mmHg for Group A and B respectively, p<0.05), haemodynamic variables were similar at baseline of each infusion and were unchanged by saline placebo infusion (p>0.05 for all). SNP, UCN2 and UCN 3 infusions increased heart rate and cardiac index, and reduced systolic and diastolic blood pressure and peripheral vascular resistance index (PVRI) in both healthy volunteers and patients with heart failure (p<0.05 for all; see Figure 1). There were no significant differences in the changes in cardiac index or PVRI between healthy volunteers and patients with heart failure during either UCN 2 or UCN 3 infusions (p>0.05). Conclusion: Intravenous UCN 2 and especially UCN 3 increase cardiac output and reduce peripheral vascular resistance. This favourable haemodynamic profile suggests that UCN 2 and UCN 3 hold exciting therapeutic potential for the treatment of acute heart failure.

Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses

1996 ◽  
Vol 80 (3) ◽  
pp. 999-1005 ◽  
Author(s):  
M. Van Soeren ◽  
T. Mohr ◽  
M. Kjaer ◽  
T. E. Graham
Keyword(s):  
Blood Pressure ◽  
Adenosine Receptors ◽  
Vascular Tissue ◽  
Physiological Responses ◽  
Acute Effects ◽  
Peripheral Vascular ◽  
Direct Stimulation ◽  
Spinal Cord Lesions ◽  
Caffeine Ingestion ◽  
Stimulation Of

Caffeine ingestion has been demonstrated to increase circulating epinephrine (Epi) and norepinephrine (NE), elevate free fatty acids (FFAs), and alter heart rate, blood pressure (BP), and ventilation in humans. Whether these physiological responses are a result of caffeine acting through direct stimulation of specific tissues via adenosine receptors or secondary to Epi increases is not known. In the present experiment, six tetraplegics (level of spinal cord lesions C4-C6) were tested at rest for 3 h to investigate the effects of 6 mg/kg caffeine in capsule form on subjects with impaired Epi responses. Ventilatory, cardiovascular, metabolic, and hormonal data were collected every 15-20 min after caffeine ingestion. There were no significant (P > 0.05) increases in plasma Epi after caffeine ingestion [0.19 +/- 0.04 (SE) nM (preingestion); 0.20 +/- 0.04 nM (80 min postingestion)] or in plasma NE [0.53 +/- 0.16 nM (preingestion); 0.49 +/- 0.09 nM (80 min postingestion; P > 0.05)]. However, significant increases were found in serum FFAs [0.53 +/- 0.08 nM (preingestion); 1.03 +/- 0.20 mM (40 min postingestion; P < 0.05] and in glycerol. These concentrations remained elevated throughout the experiment. BP increased in the first hour postingestion. These data demonstrate that caffeine in physiological doses directly stimulates specific tissues, i.e., adipose and peripheral vascular tissue, and these effects are not secondary to increases in Epi after caffeine ingestion.

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