Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reasons are given why calcium, obesity and genetics cannot be considered primary factors in the etiology of essential hypertension. This leaves the major protagonists as salt and neuroendocrine responses to the emotions aroused by the social environment. Most essential hypertension is renin dependent and associated with the physiological changes induced by arousal of the defence response. The psychosocial stimulation associated with this arousal induces an increase in salt appetite. This makes the salt consumption of society a measure of the social stress to which it is exposed. Primitive people whose blood pressure remains normal throughout their lives may lack modern societies' physically protective achievements but their religiously prescribed social solidarity may protect them from psychosocial stress. Our chronic suppression of awareness of emotional arousal together with loss of the ritualized support of affiliative behavior may result in repressed emotional responses which find somatic expression in diseases such as essential hypertension. Hypertensiologist George Pickering proposed that the primitive's ritual and taboo (the equivalent in our society might be the Alcoholic's Anonymous belief in a 'Higher Power') protect them from much anger and despair. He gave this precedence over salt as the primary factor in essential hypertension. New evidence supports this. Despite a high salt diet the blood pressure of socially adjusted rodents remains normal throughout their lifespan. On the other hand, the hypertension that develops when they are psychosocially stimulated is not abated by a low salt diet. In humans, the blood pressure of cloistered, secluded Italian nuns on a high salt diet has remained normal for 20 years while that of nearby village women has risen at a startling 2 mmHg/annum during the same period. On the other hand, in rapidly changing Malawi mature adult, rural and urban blood pressures are rising fast despite a low salt intake. Thus the evidence today argues that the most important factor in the etiology of essential hypertension is not salt but psychosocial stimulation.
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PMID:Stress, salt and hypertension. 327 18

The incidence of depression doubles in diabetic patients and is associated with poor outcomes. Studies indicate that renin-angiotensin-aldosterone system inhibitors (RAASi) might relieve depression, however the mechanism of action is not well understood. We recently showed that angiotensin receptor blockers have antidepressant effects in experimental diabetes comorbid depression. Here we investigated whether all types of RAASi exhibit antidepressant and neuroprotective properties. Diabetes was induced by streptozotocin in adult male Wistar rats. After 5 weeks of diabetes, rats were treated per os with non-pressor doses of enalapril, ramipril, spironolactone or eplerenone for 2 weeks. Behavior was evaluated using forced swim test and open field test. Inflammatory response and brain-derived neurotrophic factor (BDNF) signaling were investigated in the hippocampus. Both ACEi and MR antagonists reversed diabetes-induced behavioral despair confirming their antidepressant-like effect. This may occur via alterations in hippocampal cytokine-mediated inflammatory response. Repressed BDNF production was restored by RAASi. Both ACEi and MR antagonists facilitated the BDNF-tropomyosin receptor kinase B-cAMP response element-binding protein signaling pathway as part of their neuroprotective effect. These data highlight the important benefits of ACEi and MR antagonists in the treatment of diabetes-associated depressive symptoms. Our novel findings support the link between diabetes comorbid depression, inflammation and repressed BDNF signaling. RAASi could provide new therapeutic options to improve the outcomes of both disorders.
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PMID:Antidepressant effect in diabetes-associated depression: A novel potential of RAAS inhibition. 3244 76