The reactivity of vascular smooth muscle in helical strips from femoral arteries of normotensive, spontaneously hypertensive, renal hypertensive, and deoxycorticosterone acetate-(DCA-) hypertensive rats was studied. Spontaneous rhythmic contractions occurred in 25 of the 30 strips from the three groups of hypertensive rats and in only 2 of the 10 strips from normotensive rats. Strips from renal and DCAhypertensive rats had lower thresholds to epinephrine and potassium chloride (KC1) than did strips from spontaneously hypertensive and normotensive rats. Lanthanum (2.5 HIM) caused contraction of all 10 strips from spontaneously hypertensive rats but failed to cause contraction of any strip from the other three groups of rats. Strontium (5 mvc) caused contraction in 8 of 10 strips from spontaneously hypertensive rats but caused contraction in only 7 of the 30 strips from the other three groups. The optimal calcium concentration for tension development in response to a KC1 stimulus was approximately twice as high for strips from hypertensive rats as it was for strips from normotensive rats. Strips from DCA-hypertensive rats showed less tachyphylaxis to angiotensin II than did strips from the other three groups of rats. These results quantify our earlier observation that the reactivity of vascular smooth muscle from hypertensive rats is importantly different from that of normotensive rats. In addition, the study delineates individuality in vascular smooth muscle reactivity in different types of experimental hypertension. The results suggest that the cell membrane of the vascular smooth muscle in the hypertensive rat is more labile than that in the normal rat. KEY WORDSrenal hypertension DCA-hypertension angiotensin spontaneously hypertensive rats calcium artery strip lanthanum strontium From the Department of Physiology, University of Michigan, Ann Arbor, Michigan 48104.
a t 3 112 mos. w i t h hepatomegaly, hypoglycemia, l a c t i c a c i d o s i s , hyperuricemia, cholesterol and t r i g l y c e r i d e s . She a l s o had s y s t o l i c HP, B.P. v a r y i n g between 140-200 nrm Hg. Glucagon s t i mu l a t i o n caused paradoximal hypoglycemia. Light and e l e c t r o n microscopy of l i v e r biopsy were c o n s i s t e n t w i t h GSD. Enzyme a s s a y s ( c o u r t e s y of Dr. G. Hug) revealed t h e following: G6-PI--t a s e 5.6 u moles P/min/g t i s s u e (N = 4.7 + 1 . 9 ) ; l i v e r and musc l e debrancher enzyme was p r e s e n t ; l i v e r phosphorylase was 12.0 u moles Plminlg t i s s u e (N = 25.1 + 6 . 5 ) ; a c t i v e muscle phosphory l a s e was 9.71 (N = 47.7 + 13.2) and t o t a l muscle phosphorylase was 53.5 (N = 78.0 f 21.1); l i v e r phosphorylase k i n a s e was 0.06; n moles b---) a/min/mg T r o t . (N = 0.175 + 0.068). Catecholamine s , VMA, HVA, 17-OH, 17-KS, Aldosterone, plasma r e n i n , Ccr, IVP, and aortogram were a l l normal. At 11 mos. she developed general i z e d xanthomas; serum c h o l e s t e r o l was 906 mg% and t r i g l y c e r i d e s 3620 mg%. C l o f i b r a t e was s t a r t e d and a month l a t e r t h e r e was r e s o l u t i o n of h e r xanthomas w i t h f a l l i n c h o l e s t e r o l t o 259 mg% and t r i g l y c e r i d e s t o 1624 mg%. P r e s e n t l y she i s being maintained on p r o p r a I n t h e syndrome of f a m i l i a l dwarfism w i t h high plasma immunor e a c t i v e growth hormone (GH)(Laron Syndrome), e l e v a t e d l e v e l s ol GH a r e a s s o c i a t e d w i t h low l e v e l s of plasma somatomedin t h a t do n o t i n c r e a s e f o l l o w i n g a d m i n i s t r a t i o n of GH.These p a t i e n t s do n o t respond t o t r e a t m e n t w i t h GH.The two s u b j e c t s of t h i s r e p o r t were three-year-old boys wit1 dwarfism ( h e i g h t ages 1 3/12 and 1 6/12 y e a r s ) and delayed bone ages ( 1 3/12 and 1 9/12 y e a r s ) . Both had normal GH response a f t e r s t i m u l a t i o n a s s o c i a t e d w i t h u n d e t e c t a b l e l e v e l s of somato. medin. However, u n l i k e p a t i e n t s w i t h Laron Syndrome, t h e two p a t i e n t s generated normal l e v e l s of somatomedin a f t e r i n t r amuscular a d m i n i s t r a t i o n of GH.Treatment w i t h G H ( 2 IU every o t h e r day) brought a s i g n i f i c a n t i n c r e a s e i n t h e growth r a t e of both p a t i e n t s . The growth r a t e of t h e f i r s t p a t i e n t increased from 2 cmIyear b e f o r e t r e a t m e n t , t o 16 cmlyear on therapy. The growth r a t e o f t h e second p a t i e n t was 4.5 cm/year b e f o r e t r e a tment, and 11.0 cm/year w h i l e on t r e a t m e n t .The two c a s e s r e p r e s e n t a new syndrome of dwarfism due t o b i o l o g i c a l l y i n a c t i v e , immunoreactive GH.I f erroneously diagnosed a s having Laron Syndrome, t h e s e p a t i e n t s may b e denied t h e b e n e f i t of treatment.f whether hGH therapy Growth r a t e s in c m / y e a r...
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