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Query: UNIPROT:P01185 (
vasopressin
)
23,126
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cardiac rehabilitation (CR) plays an important role in
cardiovascular disease
prevention. Understanding the key component of CR such as training intensity and biomarkers reflecting cardiopulmonary functions may help to better target the rehabilitation program. Thirty-four consecutive patients with coronary artery disease after percutaneous coronary intervention participated in the CR program. The difference between intervention group and control group was mainly the training intensity. Cardiopulmonary exercise testing (CPET) and blood biomarker measurements were performed before and after CR. The results demonstrated that it was safe and feasible to perform CR, while sufficient training intensity was required to significantly ameliorate CPET parameters. Among numerous biomarkers tested,
vasopressin
surrogate marker copeptin (CPP) improved significantly after CR. Moreover, improved CPP was correlated with exercise intensity and peak oxygen uptake, two most important indicators of cardiopulmonary exercise capacities. Therefore, CR may have a novel role in maintaining plasma osmolality and cardiovascular homeostasis. Graphical Abstract Cardiac rehabilitation training improves cardiopulmonary exercise parameters El and PVO
2
which are correlated with reduced CPP level. CPP, copeptin; El, exercise intensity; POV2, peak oxygen uptake.
...
PMID:Cardiac Rehabilitation with Targeted Intensity Improves Cardiopulmonary Functions Accompanying with Reduced Copeptin Level in Patients with Coronary Artery Disease. 3261 11
Chronic kidney disease (CKD) causes salt-sensitive hypertension that is often resistant to treatment and contributes to the progression of kidney injury and
cardiovascular disease
. A better understanding of the mechanisms contributing to salt-sensitive hypertension in CKD is essential to improve these outcomes. This review critically explores these mechanisms by focusing on how CKD affects distal nephron Na
+
reabsorption. CKD causes glomerulotubular imbalance with reduced proximal Na
+
reabsorption and increased distal Na
+
delivery and reabsorption. Aldosterone secretion further contributes to distal Na
+
reabsorption in CKD and is not only mediated by renin and K
+
but also by metabolic acidosis, endothelin-1, and
vasopressin
. CKD also activates the intrarenal renin-angiotensin system, generating intratubular angiotensin II to promote distal Na
+
reabsorption. High dietary Na
+
intake in CKD contributes to Na
+
retention by aldosterone-independent activation of the mineralocorticoid receptor mediated through Rac1. High dietary Na
+
also produces an inflammatory response mediated by T helper 17 cells and cytokines increasing distal Na
+
transport. CKD is often accompanied by proteinuria, which contains plasmin capable of activating the epithelial Na
+
channel. Thus, CKD causes both local and systemic changes that together promote distal nephron Na
+
reabsorption and salt-sensitive hypertension. Future studies should address remaining knowledge gaps, including the relative contribution of each mechanism, the influence of sex, differences between stages and etiologies of CKD, and the clinical relevance of experimentally identified mechanisms. Several pathways offer opportunities for intervention, including with dietary Na
+
reduction, distal diuretics, renin-angiotensin system inhibitors, mineralocorticoid receptor antagonists, and K
+
or H
+
binders.
...
PMID:Salt-sensitive hypertension in chronic kidney disease: distal tubular mechanisms. 3314 11
Depression is an independent non-traditional risk factor for
cardiovascular disease
and mortality. The chronic unpredictable mild stress (CMS) rat model is a validated model of depression. Within the paraventricular nucleus (PVN),
vasopressin
(VP) via V
1a
R and V
1b
R have been implicated in stress and neurocardiovascular dysregulation. We hypothesized that in conscious, unrestrained CMS rats vs control, unstressed rats, PVN VP results in elevated arterial pressure (MAP), heart rate and renal sympathetic nerve activity (RSNA) via activation of V
1a
R and/or V
1b
R. Male rats underwent four weeks of CMS or control conditions. They were then equipped with hemodynamic telemetry transmitters, PVN cannula, and left renal nerve electrode. V
1a
R or V
1b
R antagonism dose-dependently inhibited MAP after VP injection. V
1a
R or V
1b
R blockers at their ED
50
doses did not alter baseline parameters in either control or CMS rats, but attenuated the pressor response to VP microinjected into PVN by ~50%. Combined V-
1a
R and V
1b
R inhibition completely blocked the pressor response to PVN VP in control but not CMS rats. CMS rats required combined maximally inhibitory doses to block either endogenous VP within the PVN or responses to microinjected VP. Compared with unstressed control rats, CMS rats had higher plasma VP levels and greater abundance of V
1a
R and V
1b
R transcripts within PVN. Thus, the CMS rat model of depression results in higher resting MAP, heart rate and RSNA which can be mitigated by inhibition of vasopressinergic mechanisms involving both V
1a
R and V
1b
R within the PVN. Circulating VP may also play a role in the pressor response.
...
PMID:V
1a
and V
1b
Vasopressin Receptors Within the Paraventricular Nucleus Contribute to Hypertension in Male Rats Exposed to Chronic Mild Unpredictable Stress. 3326 70
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