PMID- 9756561
OWN - NLM
STAT- MEDLINE
DCOM- 19981119
LR  - 20190228
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 275
IP  - 4
DP  - 1998 Oct
TI  - Altered regulation of bladder nerve growth factor and neurally mediated 
      hyperactive voiding.
PG  - R1279-86
LID - 10.1152/ajpregu.1998.275.4.R1279 [doi]
AB  - Elevated bladder smooth muscle cell (BSMC) nerve growth factor (NGF) secretion 
      and related neuroplasticity are associated with hyperactive voiding in 
      spontaneously hypertensive rats (SHRs: hypertensive, behaviorally hyperactive), 
      compared with control Wistar-Kyotos (WKYs). We used two inbred strains (WKHT: 
      hypertensive; WKHA: hyperactive) to further investigate this phenomenon. WKHA 
      BSMCs secreted higher basal levels of NGF than WKHT BSMCs. Antagonists did 
      inhibit NGF output in WKHA but not WKHT cultures. Thus augmented basal secretion 
      of NGF cosegregates with a hyperactive phenotype, whereas a lack of regulatory 
      inhibition of NGF output cosegregates with a hypertensive phenotype. Bladder 
      norepinephrine content paralleled NGF content, with WKHTs > SHRs > WKHAs > WKYs, 
      providing evidence that a lack of inhibition is the greatest contributor to 
      elevated bladder NGF and noradrenergic innervation. Protein kinase C (PKC) 
      agonists affected NGF production differentially depending on strain, suggesting 
      that altered PKC signaling may contribute to strain differences in NGF secretion. 
      Finally, 6-h voiding frequency differed between the strains, with SHRs > WKHTs = 
      WKHAs > WKYs. Thus aspects of both the hypertensive and hyperactive phenotypes 
      may be associated with elevated SHR bladder NGF and hyperactive voiding.
FAU - Clemow, D B
AU  - Clemow DB
AD  - Department of Neuroscience, University of Virginia Health Sciences Center, 
      Charlottesville, Virginia 22908, USA.
FAU - Steers, W D
AU  - Steers WD
FAU - McCarty, R
AU  - McCarty R
FAU - Tuttle, J B
AU  - Tuttle JB
LA  - eng
GR  - DK-45179/DK/NIDDK NIH HHS/United States
GR  - DK-49431/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuropeptide Y)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 1F7A44V6OU (Colforsin)
RN  - 1WS297W6MV (Phenylephrine)
RN  - L628TT009W (Isoproterenol)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Colforsin/pharmacology
MH  - Hypertension/*physiopathology
MH  - Isoproterenol/pharmacology
MH  - Nerve Growth Factors/biosynthesis/metabolism/*physiology
MH  - Neuronal Plasticity
MH  - Neuropeptide Y/pharmacology
MH  - Phenylephrine/pharmacology
MH  - Platelet-Derived Growth Factor/pharmacology
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Species Specificity
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Urinary Bladder/drug effects/physiology/*physiopathology
MH  - Urination/*physiology
MH  - Urination Disorders/*physiopathology
EDAT- 1998/10/02 00:00
MHDA- 1998/10/02 00:01
CRDT- 1998/10/02 00:00
PHST- 1998/10/02 00:00 [pubmed]
PHST- 1998/10/02 00:01 [medline]
PHST- 1998/10/02 00:00 [entrez]
AID - 10.1152/ajpregu.1998.275.4.R1279 [doi]
PST - ppublish
SO  - Am J Physiol. 1998 Oct;275(4):R1279-86. doi: 10.1152/ajpregu.1998.275.4.R1279.