http://cardiovascres.oxfordjournals.org ... 2/318.full
The role of natriuretic peptides in cardioprotection
Atrial natriuretic peptide (ANP) and brain (B-type) natriuretic peptide (BNP) are circulating hormones of cardiac origin that play an important role in the regulation of intravascular blood volume and vascular tone. The plasma concentrations of ANP and BNP are elevated in heart failure, and they are considered to compensate for heart failure because of their diuretic, natriuretic, and vasodilating actions and inhibitory effects on renin and aldosterone secretion. Evidence is also accumulating from recent work that ANP and BNP exert their cardioprotective functions not only as circulating hormones but also as local autocrine and/or paracrine factors. In studies using cultured neonatal myocytes and fibroblasts, exogenous administration of both ANP and ANP antagonists demonstrated that ANP has antihypertrophic and antifibrotic functions. Corroborating these in vitro results, mice lacking natriuretic receptor-A (NPR-A), the receptor for ANP and BNP, develop cardiac hypertrophy and fibrosis independent of their blood pressure. Recent studies also suggest that the intracardiac natriuretic peptides/cGMP system plays a counter-regulatory role against the intracardiac renin–angiotensin–aldosterone system and TGF-beta mediated pathway. In a clinical setting, human recombinant ANP and BNP may be used for a therapy of heart failure; however, further evaluation is required in the future.
Suppression of Luteinizing Hormone Secretion by Atrial and Brain Natriuretic Peptides in Ovariectomized Rats*
JIN ZHANG, BASIL HO YUEN, W. DAVID CURRIE and PETER C. K. LEUNG†
- Author Affiliations Department of Obstetrics and Gynecology, University of British Columbia, Grace Hospital, Vancouver, British Columbia V6H 3V5 Canada
Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) are present in brain regions regulating LH secretion. Similarities in the molecular structure of these peptides suggest similar physiological function within the brain. This study examined the effects of centrally administered BNP and ANP on LH secretion in mature ovariectomized (OVX) rats. Intracerebroventricular (icv) administration of 2 nmol ANP or BNP decreased mean plasma LH concentration and LH pulse amplitude (P < 0.05 for ANP; P < 0.01 for BNP; n = 8/group) and frequency (P < 0.01 for ANP and BNP). LH secretion was not affected by ANP or BNP at a lower concentration (0.2 nmol, icv; P > 0.05; n = 8/group). It was concluded that ANP and BNP may be involved in central regulation of LH secretion.
Mechanisms possibly involved in suppression of LH secretion by ANP and BNP were also examined. OVX rats were treated with an opioid antagonist, naloxone (0.5 mg, iv), 45, 75, and 105 min after ANP or BNP (2 nmol, icv). Naloxone eliminated suppression of mean plasma LH concentration and LH pulse amplitude by 2 nmol ANP and BNP (P < 0.05; n = 7/group). OVX rats were treated with a dopamine antagonist, pimozide (0.6 mg/kg, sc), 90 min before treatment with ANP or BNP (2 nmol, icv). Pimozide pretreatment blocked suppression of LH secretion by ANP or BNP (P < 0.05; n = 9/group). Naloxone alone did not affect LH secretion (P > 0.05; n = 5). It was concluded that components of ANP and BNP suppression of LH secretion may depend upon opioid and dopamine activity.
So, the ANP/BNP (which inhibit aldosterone) response to counter RAAS results in the inhibition of LH and downstream progesterone and dihydrotestosterone (which also inhibits aldosterone). Naltrexone would remedy the LH inhibition...not sure if helminth inspired LH increase would work. Will have to read through helminths again.
I wonder if that doesn't create a viscous cycle. Aldosterone burst, ANP/BNP response, reduced progesterone and dihydrotestosterone to block/inhibit aldosterone, ANP/BNP response, and on and on.