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1 y approximately 15 mm Hg, exclusively in the spontaneously hypertensive rat.
2 term reduction in high blood pressure in the spontaneously hypertensive rat.
3 id formation and renal function in the young spontaneously hypertensive rat.
4 ificantly upregulated compared with sham-RDN spontaneously hypertensive rats.
5 e similar in the kidneys of Wistar-Kyoto and spontaneously hypertensive rats.
6 pressure in response to vasoconstrictors in spontaneously hypertensive rats.
7 antagonist SC51322 reduced blood pressure in spontaneously hypertensive rats.
8 al cerebral ischemia and 24 h reperfusion in spontaneously hypertensive rats.
9 lly, AM404 reduced hyperactivity in juvenile spontaneously hypertensive rats, a putative model of att
10 n distal middle cerebral artery occlusion in spontaneously hypertensive rats, a strain representative
11 nd we have described disordered breathing in spontaneously hypertensive rats, an animal model of gene
12 ntegrity and wall pathology were examined in spontaneously hypertensive rat and chronic angiotensin I
13 ntegrity and wall pathology were examined in spontaneously hypertensive rat and chronic angiotensin I
14 lodalton protein isolated from hypertrophied spontaneously hypertensive rat and dilated cardiomyopath
15 1a(+) immune cells are dominant in the (SHR) spontaneously hypertensive rat and expand in response to
16 duced a long-term antihypertensive effect in spontaneously hypertensive rats and antifibrotic effects
17 , purified, and sequenced from the hearts of spontaneously hypertensive rats and dilated cardiomyopat
18 ivation, attenuated hypertension in both the spontaneously hypertensive rats and the chronic angioten
20 manner, with similar levels of inhibition in spontaneously hypertensive rats and Wistar-Kyoto rats; m
21 ion-induced damage than is the kidney of the spontaneously hypertensive rat, and (b) establish the fe
22 enase and the development of hypertension in spontaneously hypertensive rats, and 2) a relationship b
23 n myotrophin-induced cardiac hypertrophy, in spontaneously hypertensive rats, and in dilated cardiomy
26 antly larger increases in MAP and HR in male spontaneously hypertensive rats as compared to normotens
27 ide hydrolase (sEH) reduce blood pressure in spontaneously hypertensive rats as well as the findings
30 mmunohistochemical staining of the aortae of spontaneously hypertensive rats demonstrated strong corr
31 Wistar Kyoto rat BM, the resultant chimeric spontaneously hypertensive rats displayed significant re
32 l ester was given by daily s.c. injection to spontaneously hypertensive rats exposed to filtered air
34 (AT(1)R-AS) in a retroviral vector prevents spontaneously hypertensive rats from developing hyperten
36 in, a hypertrophic activator identified from spontaneously hypertensive rat heart and cardiomyopathic
37 an animal model of stroke, the stroke-prone spontaneously hypertensive rat, implicated the gene enco
38 tolic blood pressure (Delta=48+/-5 mm Hg) in spontaneously hypertensive rats, indicating that SNX5 de
39 d 20-HETE formation in renal microsomes from spontaneously hypertensive rats, it has been proposed th
41 the cortex and outer medulla of 1-4-week-old spontaneously hypertensive rat kidneys relative to the c
42 s chronic hypertension develops in the young spontaneously hypertensive rat, medullary Na,K-ATPase ac
44 either the overload of heart failure (or the spontaneously hypertensive rat model) or the profound un
46 rom normal (Wistar Kyoto) and hypertrophied (spontaneously hypertensive rat) rats was investigated by
48 f the cationic peptides (200mg/kgbodywt.) to spontaneously hypertensive rats resulted in a more rapid
50 oad LVH using 2 standard rat models: (1) the spontaneously hypertensive rat (SHR) and (2) aortic band
52 xygen consumption have been described in the spontaneously hypertensive rat (SHR) and may contribute
53 binant inbred (RI) strains, derived from the spontaneously hypertensive rat (SHR) and normotensive Br
54 organism, mated it with the stroke-resistant spontaneously hypertensive rat (SHR) and performed a gen
55 quantify metabolic substrate shifts with the spontaneously hypertensive rat (SHR) as a model of left
57 regulatory brain areas, was increased in the spontaneously hypertensive rat (SHR) compared to the Wis
58 in was significantly enhanced in the RVLM of spontaneously hypertensive rat (SHR) compared with normo
59 rent at physiological membrane potentials in spontaneously hypertensive rat (SHR) compared with Wista
63 IL-17 family in genetic hypertension in the spontaneously hypertensive rat (SHR) has not been invest
64 factor that stimulates myocytes growth, from spontaneously hypertensive rat (SHR) heart and patients
72 tatively the cTnI phosphorylation changes in spontaneously hypertensive rat (SHR) model of hypertensi
76 fold in renal cortical S9 fractions from the spontaneously hypertensive rat (SHR) relative to the nor
77 middle cerebral artery occlusion (tMCAO) in spontaneously hypertensive rat (SHR) resulted in signifi
82 P expression is significantly reduced in the spontaneously hypertensive rat (SHR) which could contrib
83 and SHR.WKY-Sa) derived from a cross of the spontaneously hypertensive rat (SHR) with the Wistar-Kyo
84 aintenance of elevated blood pressure in the spontaneously hypertensive rat (SHR), a genetic model fo
85 nd maintenance of high blood pressure in the spontaneously hypertensive rat (SHR), a model of primary
88 vents the development of hypertension in the spontaneously hypertensive rat (SHR), an animal model fo
96 Furthermore, antihypertensive effects in spontaneously hypertensive rats (SHR) also revealed that
97 the susceptibility of 5- to 6-month-old male spontaneously hypertensive rats (SHR) and age/sex-matche
99 edback (TGF) activity in 7-wk-old, euvolemic spontaneously hypertensive rats (SHR) and in Wistar-Kyot
100 ne rats (SHR-SP) have more brain injury than spontaneously hypertensive rats (SHR) and normotensive c
102 smutase (ECSOD) reduces arterial pressure in spontaneously hypertensive rats (SHR) and whether its he
105 myosin light chain kinase (smMLCK) by using spontaneously hypertensive rats (SHR) as an experimental
106 solated carotid body glomus cells from young spontaneously hypertensive rats (SHR) before the onset o
107 mined in DHI, Losartan, and placebo- treated Spontaneously Hypertensive Rats (SHR) by both noninvasiv
109 d renal sympathetic nerve activity (RSNA) in spontaneously hypertensive rats (SHR) compared to normot
110 red in distal mesenteric arteries from adult spontaneously hypertensive rats (SHR) compared with norm
111 ion showed greater levels of PRR mRNA in the spontaneously hypertensive rats (SHR) compared with norm
112 gher in the paraventricular nucleus (PVN) of spontaneously hypertensive rats (SHR) compared with thei
113 uscle cells (ASMCs) obtained from adult male spontaneously hypertensive rats (SHR) compared with thos
114 After a period of stable hypertrophy, male spontaneously hypertensive rats (SHR) develop heart fail
115 wever, AMPAR-EPSCs of labeled PVN neurons in spontaneously hypertensive rats (SHR) displayed inward r
120 nsive strain rats having the highest and the spontaneously hypertensive rats (SHR) having the lowest
122 ied the metabolic effects of pioglitazone in spontaneously hypertensive rats (SHR) that harbor a dele
123 d Ang II-induced inhibition of baroreflex in spontaneously hypertensive rats (SHR) versus WKY rats.
126 al behavior were examined in male and female spontaneously hypertensive rats (SHR), a commonly used a
127 evation of peripheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-
128 rted that subjects with ADHD as well as male spontaneously hypertensive rats (SHR), a strain that is
129 KY) rats with borderline hypertension and in spontaneously hypertensive rats (SHR), a widely used gen
130 responses are impaired in arterioles of male spontaneously hypertensive rats (SHR), but they are stil
133 us injection of AdECSOD(R213G) or AdECSOD in spontaneously hypertensive rats (SHR), immunostaining de
134 t regressing left ventricular hypertrophy in spontaneously hypertensive rats (SHR), possibly because
150 ransplanted into unilaterally nephrectomized spontaneously hypertensive rats (SHR-RT1.N strain) that
151 in response to increased flow, stroke-prone spontaneously hypertensive rats (SHR-SP) exhibited a sma
153 onducted on 4- to 5-week-old prehypertensive spontaneously hypertensive rats (SHRs) and age-matched n
154 N-mediated actions of Ang II are enhanced in spontaneously hypertensive rats (SHRs) and contribute to
155 aimed to observe effects of BSJYD on LVH in spontaneously hypertensive rats (SHRs) and explore its p
156 sparks in ventricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age- and
157 eurons isolated from the stellate ganglia of spontaneously hypertensive rats (SHRs) and their normote
158 corded in spinally projecting PVN neurons in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto
159 bers from normotensive Wistar-Kyoto rats and spontaneously hypertensive rats (SHRs) by cytofluorimetr
161 ker, candesartan, was orally administered to spontaneously hypertensive rats (SHRs) for 40 days, foll
162 a larger amplitude and shorter decay time in spontaneously hypertensive rats (SHRs) than in Wistar-Ky
164 vior and social interaction were examined in spontaneously hypertensive rats (SHRs), a commonly used
165 tivity of spinally projecting PVN neurons in spontaneously hypertensive rats (SHRs), but not in normo
168 study, we examined conditioned inhibition in spontaneously hypertensive rats (SHRs), the most well-va
178 eart rate (HR), observed in the stroke-prone spontaneously hypertensive rat (SHRSP(HD)), is a primary
181 icroangiopathy in salt-loaded, stroke-prone, spontaneously hypertensive rats (SHRSP) without controll
183 m channel blocker, SNX-111, was evaluated in spontaneously hypertensive rats subjected to 60 min of f
184 greater renal vasoconstriction in 7-wk-old, spontaneously hypertensive rats than in Wistar-Kyoto rat
186 izes the authors' recent experience with the spontaneously hypertensive rat, the best experimental mo
190 e used an animal model of ischemic stroke in spontaneously hypertensive rats to determine whether or
192 blood pressure reduction in both normal and spontaneously hypertensive rats via interactions with th
194 ithelial cells derived from Wistar-Kyoto and spontaneously hypertensive rats were grown to confluency
195 RF-RDN (n=14) or sham-RDN (n=14) treatment, spontaneously hypertensive rats were subjected to 30 min
198 od pressure in the aorta-ligated rat and the spontaneously hypertensive rat when administered orally.
199 reflex-function curves is exaggerated in the spontaneously hypertensive rat where the cardiac compone
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