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1 was also investigated in SHR (spontaneously hypertensive rats).
2 e severity of proteinuria in the Fawn-hooded hypertensive rat.
3 y 15 mm Hg, exclusively in the spontaneously hypertensive rat.
4 in high blood pressure in the spontaneously hypertensive rat.
5 s STIM1, which is up-regulated in VSMCs from hypertensive rats.
6 sympathetic-related hypothalamic neurons in hypertensive rats.
7 excitatory/inhibitory balance in the PVN of hypertensive rats.
8 al-evoked intracellular Ca(2+) transients in hypertensive rats.
9 howed a diminished dendritic surface area in hypertensive rats.
10 charge was enhanced in PVN-RVLM neurons from hypertensive rats.
11 sion nor caused postthrombotic hemorrhage in hypertensive rats.
12 nhanced steady-state current inactivation in hypertensive rats.
13 stabilized the BBB and improved mortality in hypertensive rats.
14 1322 reduced blood pressure in spontaneously hypertensive rats.
15 chemia and 24 h reperfusion in spontaneously hypertensive rats.
16 of NO and reduced portal pressure in portal hypertensive rats.
17 ion was increased in renal microvessels from hypertensive rats.
18 renal damage, was also lower in CDU-treated hypertensive rats.
19 , 3 mg/d) for 10 d lowered BP in angiotensin hypertensive rats.
20 eNOS catalytic activity in the SMA of portal hypertensive rats.
21 ased BP-CVD risk factors in normotensive and hypertensive rats.
22 VH and blood pressure (BP) in Ang II-infused hypertensive rats.
23 y that paradoxically occurs in AngII-treated hypertensive rats.
24 MC isolated from capacitance arteries of pre-hypertensive rats.
25 e and increased firing activity of MNCs from hypertensive rats.
26 re lowering effect of caloric restriction in hypertensive rats.
27 med on two-kidney, one-clip (2K1C) Goldblatt hypertensive rats.
28 od flow and portal venous pressure in portal hypertensive rats.
29 e arteries from normotensive and genetically hypertensive rats.
30 th muscle cells and aortas of Ang II-infused hypertensive rats.
31 n receptor (TR) expression and regulation in hypertensive rats.
32 he kidneys of Wistar-Kyoto and spontaneously hypertensive rats.
33 s was examined in ventricles of renovascular hypertensive rats.
34 activity in VSMCs isolated from genetically hypertensive rats.
35 flammation in the paraventricular nucleus of hypertensive rats.
36 not change hemodynamic parameters in portal hypertensive rats.
37 gulated compared with sham-RDN spontaneously hypertensive rats.
38 respiratory modulation that is amplified in hypertensive rats.
39 e stimulus magnitude in normotensive but not hypertensive rats.
40 rons in the hypothalamus in normotensive and hypertensive rats.
41 esponse to vasoconstrictors in spontaneously hypertensive rats.
42 IC) and oxidative stress within the brain of hypertensive rats.
43 otein levels were downregulated in aortae of hypertensive rats.
44 sulin resistance and BP in the spontaneously hypertensive rats.
45 hemodynamic and renal alterations of portal 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
59 d sequenced from the hearts of spontaneously hypertensive rats and dilated cardiomyopathic human tiss
60 helial dysfunction and cardiorenal injury in hypertensive rats and evaluated the effects of two class
61 e sufficient to reduce the blood pressure in hypertensive rats and justify further investigation in l
62 in sinusoidal endothelial cells from portal hypertensive rats and knockdown of GRK2 restored Akt pho
64 uated hypertension in both the spontaneously hypertensive rats and the chronic angiotensin II-infused
65 l autoregulatory capability in AngII-infused hypertensive rats and to determine the effect of chronic
66 epatocytes were harvested from spontaneously hypertensive rats and transplanted into recipient adult
67 imilar levels of inhibition in spontaneously hypertensive rats and Wistar-Kyoto rats; maximal inhibit
68 nduced cardiac hypertrophy, in spontaneously hypertensive rats, and in dilated cardiomyopathy human h
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
73 d the smMLCK promoters from normotensive and hypertensive rats as a model system to determine how CT
74 ncreases in MAP and HR in male spontaneously hypertensive rats as compared to normotensive Wistar-Kyo
76 (sEH) reduce blood pressure in spontaneously hypertensive rats as well as the findings of other inves
77 oduce greater vascular resistance changes in hypertensive rats because the system is saturated as a c
78 n days 15 and 16 of gestation) in borderline hypertensive rats (BHR) and control Wistar-Kyoto (WKY) r
82 ar in magnitude between normotensive and CIH hypertensive rats, but basal arterial pressure in CIH ra
83 terial pressure in both normotensive and CIH hypertensive rats, but they are not involved in the enha
84 l function in the paraventricular nucleus of hypertensive rats by promoting mitochondrial biogenesis
85 in-1 (ET-1), which is increased in DOCA-salt hypertensive rats, contributes to arterial superoxide ge
86 e were studied in single myocytes taken from hypertensive rats (Dahl SS/Jr) and SH-HF rats in heart f
87 ical staining of the aortae of spontaneously hypertensive rats demonstrated strong correlations betwe
88 retory responses to AT1 receptor blockade in hypertensive rats, depending on the magnitude of decreas
89 rat BM, the resultant chimeric spontaneously hypertensive rats displayed significant reduction in mea
90 g hypertension-induced heart failure in Dahl hypertensive rats dose-dependently prevents pathological
92 ascular smooth muscle cells from spontaneous hypertensive rats exhibited a marked decrease in MKP-1 i
95 To evaluate the responses to candesartan in hypertensive rats, experiments were performed 25 d after
96 ven by daily s.c. injection to spontaneously hypertensive rats exposed to filtered air or tobacco smo
97 pproximately two-fold upregulation in ocular hypertensive rat eyes and glaucomatous human donor eyes
98 nd susceptible to kidney injury (fawn-hooded hypertensive rat [FHH]) were evaluated for BP, proteinur
100 n a retroviral vector prevents spontaneously hypertensive rats from developing hypertension for life
102 ollagen fraction was also increased in 2K-1C hypertensive rats given vehicle (10.1+/-0.8%) compared w
105 phic activator identified from spontaneously hypertensive rat heart and cardiomyopathic human hearts.
106 microstructure of healthy and spontaneously hypertensive rat hearts at the ages of 12 and 24 months.
107 h the exercise-induced attenuation in MAP in hypertensive rats; however, detraining failed to complet
108 se-induced improvement in PICs in the PVN of hypertensive rats; however, the improvements in IL-10 we
109 el of stroke, the stroke-prone spontaneously hypertensive rat, implicated the gene encoding atrial na
110 essure (Delta=48+/-5 mm Hg) in spontaneously hypertensive rats, indicating that SNX5 depletion impair
111 ation in renal microsomes from spontaneously hypertensive rats, it has been proposed that increased e
114 outer medulla of 1-4-week-old spontaneously hypertensive rat kidneys relative to the corresponding l
115 rtension develops in the young spontaneously hypertensive rat, medullary Na,K-ATPase activity similar
116 , transgenic [hCETP](25) Dahl salt-sensitive hypertensive rat model of male-predominant coronary athe
118 rload of heart failure (or the spontaneously hypertensive rat model) or the profound unloading in a c
122 on systemic and regional hemodynamics in two hypertensive rat models, one genetic, the other induced
124 -4 (rat chromosome 14), from the Fawn-hooded hypertensive rat onto the August Copenhagen Irish geneti
129 n the hypertrophied heart of the genetically hypertensive rat relative to that of the aged-matched no
131 peptides (200mg/kgbodywt.) to spontaneously hypertensive rats resulted in a more rapid decrease in s
137 ion have been described in the spontaneously hypertensive rat (SHR) and may contribute to the pathoge
138 (RI) strains, derived from the spontaneously hypertensive rat (SHR) and normotensive Brown Norway (BN
139 olic substrate shifts with the spontaneously hypertensive rat (SHR) as a model of left ventricular hy
141 in areas, was increased in the spontaneously hypertensive rat (SHR) compared to the Wistar Kyoto (WKY
142 cantly enhanced in the RVLM of spontaneously hypertensive rat (SHR) compared with normotensive Wistar
143 logical membrane potentials in spontaneously hypertensive rat (SHR) compared with Wistar-Kyoto (WKY)
148 imulates myocytes growth, from spontaneously hypertensive rat (SHR) heart and patients with dilated c
157 TnI phosphorylation changes in spontaneously hypertensive rat (SHR) model of hypertensive heart disea
160 tested the hypothesis that in spontaneously hypertensive rat (SHR) NO produced centrally influences
162 cortical S9 fractions from the spontaneously hypertensive rat (SHR) relative to the normotensive Wist
163 al artery occlusion (tMCAO) in spontaneously hypertensive rat (SHR) resulted in significant increases
168 is study, we hypothesized that spontaneously hypertensive rat (SHR) vessels should have a smaller num
169 s significantly reduced in the spontaneously hypertensive rat (SHR) which could contribute to the ele
170 a) derived from a cross of the spontaneously hypertensive rat (SHR) with the Wistar-Kyoto rat (WKY) a
171 elevated blood pressure in the spontaneously hypertensive rat (SHR), a genetic model for essential hy
172 of high blood pressure in the spontaneously hypertensive rat (SHR), a model of primary hypertension.
174 lopment of hypertension in the spontaneously hypertensive rat (SHR), an animal model for primary hype
180 e, antihypertensive effects in spontaneously hypertensive rats (SHR) also revealed that oral administ
181 lity of 5- to 6-month-old male spontaneously hypertensive rats (SHR) and age/sex-matched normotensive
182 development of hypertension in spontaneously hypertensive rats (SHR) and hyperactive voiding in rats
183 ctivity in 7-wk-old, euvolemic spontaneously hypertensive rats (SHR) and in Wistar-Kyoto rats (WKY).
184 P) have more brain injury than spontaneously hypertensive rats (SHR) and normotensive controls (Wista
186 ) reduces arterial pressure in spontaneously hypertensive rats (SHR) and whether its heparin-binding
187 Cell counts were also made in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats; the
190 d body glomus cells from young spontaneously hypertensive rats (SHR) before the onset of hypertension
191 Losartan, and placebo- treated Spontaneously Hypertensive Rats (SHR) by both noninvasive and invasive
192 hetic nerve activity (RSNA) in spontaneously hypertensive rats (SHR) compared to normotensive Wistar-
193 ater levels of PRR mRNA in the spontaneously hypertensive rats (SHR) compared with normotensive Wista
194 mesenteric arteries from adult spontaneously hypertensive rats (SHR) compared with normotensive Wista
195 raventricular nucleus (PVN) of spontaneously hypertensive rats (SHR) compared with their controls, Wi
196 SMCs) obtained from adult male spontaneously hypertensive rats (SHR) compared with those from Wistar
197 od of stable hypertrophy, male spontaneously hypertensive rats (SHR) develop heart failure between 18
198 PSCs of labeled PVN neurons in spontaneously hypertensive rats (SHR) displayed inward rectification a
200 vidence in vivo indicates that spontaneously hypertensive rats (SHR) exhibit an increase in oxyradica
204 ats having the highest and the spontaneously hypertensive rats (SHR) having the lowest percentages of
205 lic effects of pioglitazone in spontaneously hypertensive rats (SHR) that harbor a deletion mutation
211 re examined in male and female spontaneously hypertensive rats (SHR), a commonly used animal model of
212 ipheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-dependent form
213 ects with ADHD as well as male spontaneously hypertensive rats (SHR), a strain that is frequently emp
214 borderline hypertension and in spontaneously hypertensive rats (SHR), a widely used genetic model of
215 impaired in arterioles of male spontaneously hypertensive rats (SHR), but they are still present in f
217 f AdECSOD(R213G) or AdECSOD in spontaneously hypertensive rats (SHR), immunostaining demonstrated bin
236 o increased flow, stroke-prone spontaneously hypertensive rats (SHR-SP) exhibited a smaller response,
238 to 5-week-old prehypertensive spontaneously hypertensive rats (SHRs) and age-matched normotensive co
239 ions of Ang II are enhanced in spontaneously hypertensive rats (SHRs) and contribute to the developme
240 rve effects of BSJYD on LVH in spontaneously hypertensive rats (SHRs) and explore its possible mechan
241 ricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age- and sex-matched W
242 d from the stellate ganglia of spontaneously hypertensive rats (SHRs) and their normotensive controls
243 ally projecting PVN neurons in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats.
244 otensive Wistar-Kyoto rats and spontaneously hypertensive rats (SHRs) by cytofluorimetric technique a
245 re-hypertensive (PH) and adult spontaneously hypertensive rats (SHRs) carotid body type I (glomus) ce
246 an, was orally administered to spontaneously hypertensive rats (SHRs) for 40 days, followed by intrav
247 tude and shorter decay time in spontaneously hypertensive rats (SHRs) than in Wistar-Kyoto (WKY) rats
250 l interaction were examined in spontaneously hypertensive rats (SHRs), a commonly used animal model o
251 tensive Wistar-Kyoto (WKY) rats, spontaneous hypertensive rats (SHRs), and SHRs treated with human re
252 ally projecting PVN neurons in spontaneously hypertensive rats (SHRs), but not in normotensive Wistar
254 between Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHRs), renal ETBR phosphorylation was
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
267 , observed in the stroke-prone spontaneously hypertensive rat (SHRSP(HD)), is a primary, genetically
269 in salt-loaded, stroke-prone, spontaneously hypertensive rats (SHRSP) without controlling hypertensi
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 ducible diabetes was crossed with the mRen27 hypertensive rat to create a novel model for heart failu
286 al model of ischemic stroke in spontaneously hypertensive rats to determine whether or not Thiopental
289 e reduction in both normal and spontaneously hypertensive rats via interactions with the CRLR/RAMP re
290 increase in blood pressure in spontaneously hypertensive rat was associated with gut pathology that
291 vely, represents an independent phenotype in hypertensive rats, we polygraphically recorded groups (n
292 ty, action potentials in PVN-RVLM neurons in hypertensive rats were broader, decayed more slowly, and
293 or sham-RDN (n=14) treatment, spontaneously hypertensive rats were subjected to 30 minutes of transi
296 n curves is exaggerated in the spontaneously hypertensive rat where the cardiac component has selecti
297 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