PMID- 19723539
OWN - NLM
STAT- MEDLINE
DCOM- 20100203
LR  - 20131121
IS  - 1879-016X (Electronic)
IS  - 0163-7258 (Linking)
VI  - 124
IP  - 3
DP  - 2009 Dec
TI  - Exploiting cGMP-based therapies for the prevention of left ventricular 
      hypertrophy: NO* and beyond.
PG  - 279-300
LID - 10.1016/j.pharmthera.2009.08.001 [doi]
AB  - Left ventricular hypertrophy (LVH), an increased left ventricular (LV) mass, is 
      common to many cardiovascular disorders, initially developing as an adaptive 
      response to maintain myocardial function. In the longer term, this LV remodelling 
      becomes maladaptive, with progressive decline in LV contractility and diastolic 
      function. Indeed LVH is recognised as an important blood-pressure independent 
      predictor of cardiovascular morbidity and mortality. The clinical efficacy of 
      current treatments for LVH is reduced, however, by their tendency to slow disease 
      progression rather than induce its reversal, and thus the development of new 
      therapies for LVH is paramount. The signalling molecule cyclic 
      guanosine-3',5'-monophosphate (cGMP), well-recognised for its role in regulating 
      vascular tone, is now being increasingly identified as an important 
      anti-hypertrophic mediator. This review is focused on the various means by which 
      cGMP can be stimulated in the heart, such as via the natriuretic peptides, to 
      exert anti-hypertrophic actions. In particular we address the limitations of 
      traditional nitric oxide (NO*) donors in the face of the potential therapeutic 
      advantages offered by novel alternatives; NO* siblings, ligands of the 
      cGMP-generating enzymes, soluble (sGC) and particulate guanylyl cyclases (pGC), 
      and phosphodiesterase inhibitors. Further impact of cGMP within the 
      cardiovascular system is also discussed with a view to representing cGMP-based 
      therapies as innovative pharmacotherapy, alone or concurrent with standard care, 
      for the management of LVH.
FAU - Ritchie, Rebecca H
AU  - Ritchie RH
AD  - Heart Failure Pharmacology, Baker IDI Heart & Diabetes Institute Melbourne, 
      Victoria, Australia. rebecca.ritchie@bakeridi.edu.au
FAU - Irvine, Jennifer C
AU  - Irvine JC
FAU - Rosenkranz, Anke C
AU  - Rosenkranz AC
FAU - Patel, Ruchi
AU  - Patel R
FAU - Wendt, Igor R
AU  - Wendt IR
FAU - Horowitz, John D
AU  - Horowitz JD
FAU - Kemp-Harper, Barbara K
AU  - Kemp-Harper BK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20090829
PL  - England
TA  - Pharmacol Ther
JT  - Pharmacology & therapeutics
JID - 7905840
RN  - 0 (Natriuretic Peptides)
RN  - 0 (Nitric Oxide Donors)
RN  - 0 (Phosphodiesterase Inhibitors)
RN  - 7U1EE4V452 (Carbon Monoxide)
RN  - EC 4.6.1.2 (Guanylate Cyclase)
RN  - H2D2X058MU (Cyclic GMP)
SB  - IM
MH  - Carbon Monoxide/physiology
MH  - Cardiovascular System/metabolism/physiopathology
MH  - Cyclic GMP/*biosynthesis
MH  - Guanylate Cyclase/biosynthesis/therapeutic use
MH  - Humans
MH  - Hypertrophy, Left Ventricular/*drug therapy/etiology/*prevention & control
MH  - Natriuretic Peptides/therapeutic use
MH  - Nitric Oxide Donors/*therapeutic use
MH  - Phosphodiesterase Inhibitors/therapeutic use
RF  - 361
EDAT- 2009/09/03 06:00
MHDA- 2010/02/04 06:00
CRDT- 2009/09/03 09:00
PHST- 2009/08/14 00:00 [received]
PHST- 2009/08/14 00:00 [accepted]
PHST- 2009/09/03 09:00 [entrez]
PHST- 2009/09/03 06:00 [pubmed]
PHST- 2010/02/04 06:00 [medline]
AID - S0163-7258(09)00171-5 [pii]
AID - 10.1016/j.pharmthera.2009.08.001 [doi]
PST - ppublish
SO  - Pharmacol Ther. 2009 Dec;124(3):279-300. doi: 10.1016/j.pharmthera.2009.08.001. 
      Epub 2009 Aug 29.