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1 y 15 mm Hg, exclusively in the spontaneously hypertensive rat.
2 in high blood pressure in the spontaneously hypertensive rat.
3 nd renal function in the young spontaneously hypertensive rat.
4 e severity of proteinuria in the Fawn-hooded hypertensive rat.
5 al-evoked intracellular Ca(2+) transients in hypertensive rats.
6 howed a diminished dendritic surface area in hypertensive rats.
7 charge was enhanced in PVN-RVLM neurons from hypertensive rats.
8 sion nor caused postthrombotic hemorrhage in hypertensive rats.
9 nhanced steady-state current inactivation in hypertensive rats.
10 stabilized the BBB and improved mortality in hypertensive rats.
11 1322 reduced blood pressure in spontaneously hypertensive rats.
12 chemia and 24 h reperfusion in spontaneously hypertensive rats.
13 of NO and reduced portal pressure in portal hypertensive rats.
14 ion was increased in renal microvessels from hypertensive rats.
15 renal damage, was also lower in CDU-treated hypertensive rats.
16 , 3 mg/d) for 10 d lowered BP in angiotensin hypertensive rats.
17 eNOS catalytic activity in the SMA of portal hypertensive rats.
18 ased BP-CVD risk factors in normotensive and hypertensive rats.
19 VH and blood pressure (BP) in Ang II-infused hypertensive rats.
20 y that paradoxically occurs in AngII-treated hypertensive rats.
21 flammation in the paraventricular nucleus of hypertensive rats.
22 MC isolated from capacitance arteries of pre-hypertensive rats.
23 not change hemodynamic parameters in portal hypertensive rats.
24 re lowering effect of caloric restriction in hypertensive rats.
25 med on two-kidney, one-clip (2K1C) Goldblatt hypertensive rats.
26 gulated compared with sham-RDN spontaneously hypertensive rats.
27 od flow and portal venous pressure in portal hypertensive rats.
28 e arteries from normotensive and genetically hypertensive rats.
29 th muscle cells and aortas of Ang II-infused hypertensive rats.
30 n receptor (TR) expression and regulation in hypertensive rats.
31 he kidneys of Wistar-Kyoto and spontaneously hypertensive rats.
32 s was examined in ventricles of renovascular hypertensive rats.
33 activity in VSMCs isolated from genetically hypertensive rats.
34 sculature in both groups, but less in portal hypertensive rats.
35 tral blood volume in Na+ retention in portal hypertensive rats.
36 e and increased firing activity of MNCs from hypertensive rats.
37 respiratory modulation that is amplified in hypertensive rats.
38 e stimulus magnitude in normotensive but not hypertensive rats.
39 rons in the hypothalamus in normotensive and hypertensive rats.
40 esponse to vasoconstrictors in spontaneously hypertensive rats.
41 IC) and oxidative stress within the brain of hypertensive rats.
42 otein levels were downregulated in aortae of hypertensive rats.
43 hemodynamic and renal alterations of portal hypertensive rats.
44 sympathetic-related hypothalamic neurons in hypertensive rats.
45 excitatory/inhibitory balance in the PVN of hypertensive rats.
46 dney glomerular function in FHH (fawn-hooded hypertensive) rat.
47 nerve discharges in normotensive, but not in hypertensive, rats.
48 uced hyperactivity in juvenile spontaneously hypertensive rats, a putative model of attention deficit
49 e cerebral artery occlusion in spontaneously hypertensive rats, a strain representative of the transi
50 or 4 days), which were normotensive, and Ang-hypertensive rats (AHR; 240 microg/kg per hour for 28 da
51 cribed disordered breathing in spontaneously hypertensive rats, an animal model of genetic hypertensi
52 all pathology were examined in spontaneously hypertensive rat and chronic angiotensin II infusion rat
53 all pathology were examined in spontaneously hypertensive rat and chronic angiotensin II infusion rat
54 ells are dominant in the (SHR) spontaneously hypertensive rat and expand in response to nicotinic cho
55 evant brain areas) in two genetic strains of hypertensive rats and (2) analyze the role of adducins i
56 erm antihypertensive effect in spontaneously hypertensive rats and antifibrotic effects in isoprotere
58 d sequenced from the hearts of spontaneously hypertensive rats and dilated cardiomyopathic human tiss
59 helial dysfunction and cardiorenal injury in hypertensive rats and evaluated the effects of two class
60 in sinusoidal endothelial cells from portal hypertensive rats and knockdown of GRK2 restored Akt pho
62 uated hypertension in both the spontaneously hypertensive rats and the chronic angiotensin II-infused
63 l autoregulatory capability in AngII-infused hypertensive rats and to determine the effect of chronic
64 epatocytes were harvested from spontaneously hypertensive rats and transplanted into recipient adult
65 imilar levels of inhibition in spontaneously hypertensive rats and Wistar-Kyoto rats; maximal inhibit
66 mage than is the kidney of the spontaneously hypertensive rat, and (b) establish the feasibility of u
67 nduced cardiac hypertrophy, in spontaneously hypertensive rats, and in dilated cardiomyopathy human h
68 vascular hyporeactivity in prehepatic portal-hypertensive rats, and octreotide does not exert its act
70 (RVLM)-projecting PVN neurones is altered in hypertensive rats, and whether such changes affected sin
71 indings indicate that HO-1 is upregulated in hypertensive rat aortas, apparently by mechanisms unique
74 d the smMLCK promoters from normotensive and hypertensive rats as a model system to determine how CT
75 ncreases in MAP and HR in male spontaneously hypertensive rats as compared to normotensive Wistar-Kyo
77 (sEH) reduce blood pressure in spontaneously hypertensive rats as well as the findings of other inves
78 oduce greater vascular resistance changes in hypertensive rats because the system is saturated as a c
79 n days 15 and 16 of gestation) in borderline hypertensive rats (BHR) and control Wistar-Kyoto (WKY) r
83 ar in magnitude between normotensive and CIH hypertensive rats, but basal arterial pressure in CIH ra
84 terial pressure in both normotensive and CIH hypertensive rats, but they are not involved in the enha
85 l function in the paraventricular nucleus of hypertensive rats by promoting mitochondrial biogenesis
87 in-1 (ET-1), which is increased in DOCA-salt hypertensive rats, contributes to arterial superoxide ge
88 e were studied in single myocytes taken from hypertensive rats (Dahl SS/Jr) and SH-HF rats in heart f
89 ical staining of the aortae of spontaneously hypertensive rats demonstrated strong correlations betwe
90 retory responses to AT1 receptor blockade in hypertensive rats, depending on the magnitude of decreas
91 rat BM, the resultant chimeric spontaneously hypertensive rats displayed significant reduction in mea
92 g hypertension-induced heart failure in Dahl hypertensive rats dose-dependently prevents pathological
94 ascular smooth muscle cells from spontaneous hypertensive rats exhibited a marked decrease in MKP-1 i
97 To evaluate the responses to candesartan in hypertensive rats, experiments were performed 25 d after
98 ven by daily s.c. injection to spontaneously hypertensive rats exposed to filtered air or tobacco smo
99 pproximately two-fold upregulation in ocular hypertensive rat eyes and glaucomatous human donor eyes
100 nd susceptible to kidney injury (fawn-hooded hypertensive rat [FHH]) were evaluated for BP, proteinur
102 n a retroviral vector prevents spontaneously hypertensive rats from developing hypertension for life
104 ollagen fraction was also increased in 2K-1C hypertensive rats given vehicle (10.1+/-0.8%) compared w
107 phic activator identified from spontaneously hypertensive rat heart and cardiomyopathic human hearts.
108 h the exercise-induced attenuation in MAP in hypertensive rats; however, detraining failed to complet
109 se-induced improvement in PICs in the PVN of hypertensive rats; however, the improvements in IL-10 we
110 el of stroke, the stroke-prone spontaneously hypertensive rat, implicated the gene encoding atrial na
111 essure (Delta=48+/-5 mm Hg) in spontaneously hypertensive rats, indicating that SNX5 depletion impair
112 ation in renal microsomes from spontaneously hypertensive rats, it has been proposed that increased e
115 outer medulla of 1-4-week-old spontaneously hypertensive rat kidneys relative to the corresponding l
116 rtension develops in the young spontaneously hypertensive rat, medullary Na,K-ATPase activity similar
117 , transgenic [hCETP](25) Dahl salt-sensitive hypertensive rat model of male-predominant coronary athe
119 rload of heart failure (or the spontaneously hypertensive rat model) or the profound unloading in a c
123 on systemic and regional hemodynamics in two hypertensive rat models, one genetic, the other induced
126 -4 (rat chromosome 14), from the Fawn-hooded hypertensive rat onto the August Copenhagen Irish geneti
131 n the hypertrophied heart of the genetically hypertensive rat relative to that of the aged-matched no
133 ty of K(Ca) and K(v) channels are altered in hypertensive rat renal interlobar arteries and may play
134 peptides (200mg/kgbodywt.) to spontaneously hypertensive rats resulted in a more rapid decrease in s
140 ion have been described in the spontaneously hypertensive rat (SHR) and may contribute to the pathoge
141 (RI) strains, derived from the spontaneously hypertensive rat (SHR) and normotensive Brown Norway (BN
142 olic substrate shifts with the spontaneously hypertensive rat (SHR) as a model of left ventricular hy
144 in areas, was increased in the spontaneously hypertensive rat (SHR) compared to the Wistar Kyoto (WKY
145 cantly enhanced in the RVLM of spontaneously hypertensive rat (SHR) compared with normotensive Wistar
146 logical membrane potentials in spontaneously hypertensive rat (SHR) compared with Wistar-Kyoto (WKY)
151 imulates myocytes growth, from spontaneously hypertensive rat (SHR) heart and patients with dilated c
159 TnI phosphorylation changes in spontaneously hypertensive rat (SHR) model of hypertensive heart disea
162 tested the hypothesis that in spontaneously hypertensive rat (SHR) NO produced centrally influences
164 cortical S9 fractions from the spontaneously hypertensive rat (SHR) relative to the normotensive Wist
165 al artery occlusion (tMCAO) in spontaneously hypertensive rat (SHR) resulted in significant increases
170 s significantly reduced in the spontaneously hypertensive rat (SHR) which could contribute to the ele
171 a) derived from a cross of the spontaneously hypertensive rat (SHR) with the Wistar-Kyoto rat (WKY) a
172 elevated blood pressure in the spontaneously hypertensive rat (SHR), a genetic model for essential hy
173 of high blood pressure in the spontaneously hypertensive rat (SHR), a model of primary hypertension.
176 lopment of hypertension in the spontaneously hypertensive rat (SHR), an animal model for primary hype
184 e, antihypertensive effects in spontaneously hypertensive rats (SHR) also revealed that oral administ
185 lity of 5- to 6-month-old male spontaneously hypertensive rats (SHR) and age/sex-matched normotensive
186 development of hypertension in spontaneously hypertensive rats (SHR) and hyperactive voiding in rats
187 ctivity in 7-wk-old, euvolemic spontaneously hypertensive rats (SHR) and in Wistar-Kyoto rats (WKY).
188 P) have more brain injury than spontaneously hypertensive rats (SHR) and normotensive controls (Wista
190 ) reduces arterial pressure in spontaneously hypertensive rats (SHR) and whether its heparin-binding
191 Cell counts were also made in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats; the
194 d body glomus cells from young spontaneously hypertensive rats (SHR) before the onset of hypertension
195 Losartan, and placebo- treated Spontaneously Hypertensive Rats (SHR) by both noninvasive and invasive
196 hemic tolerance was induced in spontaneously hypertensive rats (SHR) by injection of a single dose of
197 hetic nerve activity (RSNA) in spontaneously hypertensive rats (SHR) compared to normotensive Wistar-
198 mesenteric arteries from adult spontaneously hypertensive rats (SHR) compared with normotensive Wista
199 ater levels of PRR mRNA in the spontaneously hypertensive rats (SHR) compared with normotensive Wista
200 raventricular nucleus (PVN) of spontaneously hypertensive rats (SHR) compared with their controls, Wi
201 SMCs) obtained from adult male spontaneously hypertensive rats (SHR) compared with those from Wistar
202 od of stable hypertrophy, male spontaneously hypertensive rats (SHR) develop heart failure between 18
203 PSCs of labeled PVN neurons in spontaneously hypertensive rats (SHR) displayed inward rectification a
205 vidence in vivo indicates that spontaneously hypertensive rats (SHR) exhibit an increase in oxyradica
208 ats having the highest and the spontaneously hypertensive rats (SHR) having the lowest percentages of
210 lic effects of pioglitazone in spontaneously hypertensive rats (SHR) that harbor a deletion mutation
214 re examined in male and female spontaneously hypertensive rats (SHR), a commonly used animal model of
215 ipheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-dependent form
216 ects with ADHD as well as male spontaneously hypertensive rats (SHR), a strain that is frequently emp
217 borderline hypertension and in spontaneously hypertensive rats (SHR), a widely used genetic model of
218 impaired in arterioles of male spontaneously hypertensive rats (SHR), but they are still present in f
221 f AdECSOD(R213G) or AdECSOD in spontaneously hypertensive rats (SHR), immunostaining demonstrated bin
237 to unilaterally nephrectomized spontaneously hypertensive rats (SHR-RT1.N strain) that harbor the maj
238 o increased flow, stroke-prone spontaneously hypertensive rats (SHR-SP) exhibited a smaller response,
240 to 5-week-old prehypertensive spontaneously hypertensive rats (SHRs) and age-matched normotensive co
241 ions of Ang II are enhanced in spontaneously hypertensive rats (SHRs) and contribute to the developme
242 rve effects of BSJYD on LVH in spontaneously hypertensive rats (SHRs) and explore its possible mechan
243 ricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age- and sex-matched W
244 d from the stellate ganglia of spontaneously hypertensive rats (SHRs) and their normotensive controls
245 ally projecting PVN neurons in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats.
246 otensive Wistar-Kyoto rats and spontaneously hypertensive rats (SHRs) by cytofluorimetric technique a
247 re-hypertensive (PH) and adult spontaneously hypertensive rats (SHRs) carotid body type I (glomus) ce
248 an, was orally administered to spontaneously hypertensive rats (SHRs) for 40 days, followed by intrav
249 tude and shorter decay time in spontaneously hypertensive rats (SHRs) than in Wistar-Kyoto (WKY) rats
251 l interaction were examined in spontaneously hypertensive rats (SHRs), a commonly used animal model o
252 tensive Wistar-Kyoto (WKY) rats, spontaneous hypertensive rats (SHRs), and SHRs treated with human re
253 ally projecting PVN neurons in spontaneously hypertensive rats (SHRs), but not in normotensive Wistar
255 ese effects are exaggerated in spontaneously hypertensive rats (SHRs), resulting in an augmented CO2
256 ined conditioned inhibition in spontaneously hypertensive rats (SHRs), the most well-validated animal
266 , observed in the stroke-prone spontaneously hypertensive rat (SHRSP(HD)), is a primary, genetically
268 in salt-loaded, stroke-prone, spontaneously hypertensive rats (SHRSP) without controlling hypertensi
270 found by linkage in experimental hereditary hypertensive rat strains, but their relationship to huma
271 ker, SNX-111, was evaluated in spontaneously hypertensive rats subjected to 60 min of focal cerebral
272 phenotypically normotensive but genetically hypertensive rats suggests that disordered breathing rep
274 optic nucleus and paraventricular nucleus of hypertensive rats that contributes to neurohumoral activ
275 , in ventricular myocytes from spontaneously hypertensive rats that develop heart failure, we identif
276 ic hypertension model in Dahl salt-sensitive hypertensive rats that overexpress the human cholesteryl
277 rs' recent experience with the spontaneously hypertensive rat, the best experimental model for natura
278 e MCAO model, conducted in the spontaneously hypertensive rat, the more polar 3-hydroxy derivative (+
279 cated in disease in studies with genetically hypertensive rats, the microsatellite markers reported h
281 After oral administration to spontaneously hypertensive rats, the S1P1 selective compound 85 showed
282 tive cells were increased in the LV of 2K-1C hypertensive rats; this increase was significantly blunt
283 e superior mesenteric arterial bed of portal hypertensive rats through direct measurement of NO metab
284 bioinformatics and genomic techniques, Milan hypertensive rat tissues were studied because this strai
285 al model of ischemic stroke in spontaneously hypertensive rats to determine whether or not Thiopental
287 e reduction in both normal and spontaneously hypertensive rats via interactions with the CRLR/RAMP re
288 increase in blood pressure in spontaneously hypertensive rat was associated with gut pathology that
289 vely, represents an independent phenotype in hypertensive rats, we polygraphically recorded groups (n
290 ty, action potentials in PVN-RVLM neurons in hypertensive rats were broader, decayed more slowly, and
291 derived from Wistar-Kyoto and spontaneously hypertensive rats were grown to confluency on semipermea
292 or sham-RDN (n=14) treatment, spontaneously hypertensive rats were subjected to 30 minutes of transi
295 n curves is exaggerated in the spontaneously hypertensive rat where the cardiac component has selecti
296 tochondrial structural disarray in brains of hypertensive rats with hypertension-induced brain injury
299 ration, and collagen deposition in the LV of hypertensive rats without affecting blood pressure or ca
300 to ET (10 microg/kg intravenously) in portal hypertensive rats without any significant change in plas
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